Volume 12, Issue 23

Regulation of glucose homeostasis by calorie restriction and periodic fasting

Volha Mezhnina, Roman Kondratov,

https://doi.org/10.18632/aging.104217 pp 23422—23424

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Mezhnina V, Kondratov R, . Regulation of glucose homeostasis by calorie restriction and periodic fasting. . 12:23422-23424. https://doi.org/10.18632/aging.104217

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Bacteria boost host NAD metabolism

Igor Shats, Xiaoling Li,

https://doi.org/10.18632/aging.104219 pp 23425—23426

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COVID-19
Evolution of COVID-19 in patients with autoimmune rheumatic diseases

Rongrong Pang, Jun Zhao, Zhenhua Gan, Zhiliang Hu, Xiang Xue, Yanjun Wu, Qinghua Qiao, Aifang Zhong, Xinyi Xia, Hui Liao, Zhihua Wang, Libo Zhang,

https://doi.org/10.18632/aging.202193 pp 23427—23435

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Pang R, Zhao J, Gan Z, Hu Z, Xue X, Wu Y, Qiao Q, Zhong A, Xia X, Liao H, Wang Z, Zhang L, . Evolution of COVID-19 in patients with autoimmune rheumatic diseases. . 12:23427-23435. https://doi.org/10.18632/aging.202193

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Provider: 
                TY  - JOUR
                AU  - Pang, Rongrong 
                AU  - Zhao, Jun 
                AU  - Gan, Zhenhua 
                AU  - Hu, Zhiliang 
                AU  - Xue, Xiang 
                AU  - Wu, Yanjun 
                AU  - Qiao, Qinghua 
                AU  - Zhong, Aifang 
                AU  - Xia, Xinyi 
                AU  - Liao, Hui 
                AU  - Wang, Zhihua 
                AU  - Zhang, Libo 
                TI  - Evolution of COVID-19 in patients with autoimmune rheumatic diseases
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202193
                DO  - 10.18632/aging.202193
                SP  - 23427
                EP  - 23435
                PY  - 
                AB  - The characteristics of COVID-19 patients with autoimmune rheumatic diseases (AIRD) have rarely been reported. Patients with AIRD have suppressed immune defense function, which may increase their susceptibility to COVID-19. However, the immunosuppressive agents AIRD patients routinely used may be beneficial for protecting the cytokine storm caused by SARS-CoV-2. In this retrospective study, we included all confirmed cases in Huoshenshan Hospital from February 4 to April 9. Data were extracted from electronic medical records and were analyzed for clinical and laboratory features using SPSS (version 25.0). Of 3059 patients, 21 had the comorbidities with systematic lupus erythematosus (SLE) and/or rheumatoid arthritis (RA), including 5 with SLE, 15 with RA, and 1 with Rhupus. The proportion was 57.1% for severe cases, 61.9% for either severe or critical cases, and 4.8% for critical cases. The main manifestations, ARDS and ICU admission rate, as well as the mortality and length of hospital stay of COVID-19 in AIRD patients were similar to COVID-19 patients in the general population. Our preliminary experience shows that patients with AIRD tend to have a higher risk of SARS-CoV-2 infection, and may be at risk for a severe but less likely critical disease course. Further investigation is needed to understand the immunological features of these diseases.
                ER  -

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COVID-19
Clinical characteristics and fatal outcomes of hypertension in patients with severe COVID-19

Xiaocheng Cheng, Guoqiang Cai, Xuesong Wen, Lei Gao, Dan Jiang, Min Sun, Shu Qin, Jianzhong Zhou, Dongying Zhang,

https://doi.org/10.18632/aging.104019 pp 23436—23449

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Cheng X, Cai G, Wen X, Gao L, Jiang D, Sun M, Qin S, Zhou J, Zhang D, . Clinical characteristics and fatal outcomes of hypertension in patients with severe COVID-19. . 12:23436-23449. https://doi.org/10.18632/aging.104019

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                TY  - JOUR
                AU  - Cheng, Xiaocheng 
                AU  - Cai, Guoqiang 
                AU  - Wen, Xuesong 
                AU  - Gao, Lei 
                AU  - Jiang, Dan 
                AU  - Sun, Min 
                AU  - Qin, Shu 
                AU  - Zhou, Jianzhong 
                AU  - Zhang, Dongying 
                TI  - Clinical characteristics and fatal outcomes of hypertension in patients with severe COVID-19
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104019
                DO  - 10.18632/aging.104019
                SP  - 23436
                EP  - 23449
                PY  - 
                AB  - The aim of this study is to investigate clinical characteristics and fatal outcomes of hypertension as well as the role of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (ACEI/ARB) use in patients with severe coronavirus disease 2019 (COVID-19). A total of 220 (female: 51.8%) patients with severe COVID-19 were included. The mean age of included patients was 59.5 years and 70 (31.8%) patients had a history of hypertension. There were 23 patients (32.9%) receiving ACEI/ARB therapy. Patients with hypertension were older and had more comorbidities, and were more likely to suffer from severe inflammatory response and acute cardiac injury. Moreover, patients with hypertension were associated with significantly higher risk of in-hospital mortality than patients without hypertension. After adjustment of potential confounders, the independent correlation was still observed. In addition, ACEI/ARB users were associated with lower level of high-sensitivity cardiac troponin I and creatinine kinase&#x2013;myocardial band, and lower risk of acute cardiac injury than ACEI/ARB non-users. In conclusion, patients with hypertension were more likely to suffer from severe inflammatory response, acute cardiac injury and had high risk of in-hospital mortality in severe COVID-19. The use of ACEI/ARB may protect patients with COVID-19 from acute cardiac injury.
                ER  -

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COVID-19
Incidence of cerebrovascular disease as a comorbidity in patients with COVID-19: A meta-analysis

Jun Zhang, Haili Wang, Min Wei, Hengzhu Zhang, Boming Xia, Xingdong Wang, Yunlong Pei, Lun Dong, Yuping Li,

https://doi.org/10.18632/aging.104086 pp 23450—23463

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Zhang J, Wang H, Wei M, Zhang H, Xia B, Wang X, Pei Y, Dong L, Li Y, . Incidence of cerebrovascular disease as a comorbidity in patients with COVID-19: A meta-analysis. . 12:23450-23463. https://doi.org/10.18632/aging.104086

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                TY  - JOUR
                AU  - Zhang, Jun 
                AU  - Wang, Haili 
                AU  - Wei, Min 
                AU  - Zhang, Hengzhu 
                AU  - Xia, Boming 
                AU  - Wang, Xingdong 
                AU  - Pei, Yunlong 
                AU  - Dong, Lun 
                AU  - Li, Yuping 
                TI  - Incidence of cerebrovascular disease as a comorbidity in patients with COVID-19: A meta-analysis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104086
                DO  - 10.18632/aging.104086
                SP  - 23450
                EP  - 23463
                PY  - 
                AB  - It is essential to know whether COVID-19 patients have a history of cerebrovascular disease, as it may be predictive of prognosis and useful for allocation of limited medical resources. This meta-analysis was performed to assess the incidence of cerebrovascular disease as a comorbidity in COVID-19 patients. The PubMed, Cochrane Library, Embase, CNKI, WFSD, and VIP databases were systematically searched. The pooled analysis of relevant data was conducted using RevMan 5.3 software. The primary outcome was incidence of cerebrovascular disease as a comorbidity. Forty-seven studies involving 16,143 COVID-19 patients were included in this analysis. The incidences of a history of cerebrovascular disease and hypertension in COVID-19 patients were estimated to be 3.0% (95% CI, 2.0%-4.0%; P&lt;0.00001) and 23.0% (95% CI, 16.0%-29.0%; P&lt;0.00001), respectively. The incidence of dizziness/headache as the first symptom in COVID-19 patients was estimated to be 14.0% (95% CI, 8.0%-20.0%; P&lt;0.00001). Subgroup analyses indicated that country, sex ratio, and sample size are potential influencing factors affecting the incidences of cerebrovascular disease, hypertension, and dizziness/headache. These findings suggest that cerebrovascular disease is an underlying comorbidity among patients with COVID-19. In addition, patients experiencing dizziness/headache as the first symptom of COVID-19 should receive a neurological examination.
                ER  -

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COVID-19
Risk factors for COVID-19 patients with cardiac injury: pulmonary ventilation dysfunction and oxygen inhalation insufficiency are not the direct causes

Sucheng Mu, Wei Wei, Chaoyuan Jin, Ning Pu, Kaihuan Yu, Guorong Gu, Zhe Luo, Chaoyang Tong, Yi Han,

https://doi.org/10.18632/aging.104148 pp 23464—23477

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Mu S, Wei W, Jin C, Pu N, Yu K, Gu G, Luo Z, Tong C, Han Y, . Risk factors for COVID-19 patients with cardiac injury: pulmonary ventilation dysfunction and oxygen inhalation insufficiency are not the direct causes. . 12:23464-23477. https://doi.org/10.18632/aging.104148

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                TY  - JOUR
                AU  - Mu, Sucheng 
                AU  - Wei, Wei 
                AU  - Jin, Chaoyuan 
                AU  - Pu, Ning 
                AU  - Yu, Kaihuan 
                AU  - Gu, Guorong 
                AU  - Luo, Zhe 
                AU  - Tong, Chaoyang 
                AU  - Han, Yi 
                TI  - Risk factors for COVID-19 patients with cardiac injury: pulmonary ventilation dysfunction and oxygen inhalation insufficiency are not the direct causes
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104148
                DO  - 10.18632/aging.104148
                SP  - 23464
                EP  - 23477
                PY  - 
                AB  - Background: Cardiac injury in patients with coronavirus disease 2019 (COVID-19) has been reported in recent studies. However, reports on the risk factors for cardiac injury and their prognostic value are limited.
                Results: In total, 15.9% of all cases were defined as cardiac injury in our study. Patients with severe COVID-19 were significantly associated with older age and higher respiratory rates, Sequential Organ Failure Assessment (SOFA) scores, cardiac injury biomarkers and PaO2/FiO2 ratios. Male patients with chest distress and dyspnea were more likely to have severe disease. Patients with cardiac injury were significantly more likely to have a severe condition and have an outcome of death. However, no significant difference was found in respiratory rates, dyspnea or PaO2/FiO2 ratio between patients with or without cardiac injury. In the logistic regression model, pre-existing hypertension and higher SOFA score were independent risk factors for patients with COVID-19 developing cardiac injury.
                Conclusions: Our study revealed that cardiac injury was an important predictor for patients having a severe or fatal outcome. Patients with pre-existing hypertension and higher SOFA scores upon admission were more likely to develop cardiac injury. Nevertheless, pulmonary ventilation dysfunction and oxygen inhalation insufficiency were not the main causes of cardiac injury in patients with COVID-19.
                Methods: A total of 113 confirmed cases were included in our study. Severe patients were defined according to American Thoracic Society guidelines for community-acquired pneumonia. Cardiac injury was defined as a serum cTnI above the 99th-percentile of the upper reference limit. Patient characteristics, clinical laboratory data and treatment details were collected and analyzed. The risk factors for patients with and without cardiac injury were analyzed.
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Transforming growth factor beta type 1 (TGF-β) and hypoxia-inducible factor 1 (HIF-1) transcription complex as master regulators of the immunosuppressive protein galectin-9 expression in human cancer and embryonic cells

Anette Teo Hansen Selnø, Stephanie Schlichtner, Inna M. Yasinska, Svetlana S. Sakhnevych, Walter Fiedler, Jasmin Wellbrock, Elena Klenova, Ludmila Pavlova, Bernhard F. Gibbs, Martin Degen, Isabelle Schnyder, Nijas Aliu, Steffen M. Berger, Elizaveta Fasler-Kan, Vadim V. Sumbayev,

https://doi.org/10.18632/aging.202343 pp 23478—23496

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Selnø ATH, Schlichtner S, Yasinska IM, Sakhnevych SS, Fiedler W, Wellbrock J, Klenova E, Pavlova L, Gibbs BF, Degen M, Schnyder I, Aliu N, Berger SM, et al, . Transforming growth factor beta type 1 (TGF-β) and hypoxia-inducible factor 1 (HIF-1) transcription complex as master regulators of the immunosuppressive protein galectin-9 expression in human cancer and embryonic cells. . 12:23478-23496. https://doi.org/10.18632/aging.202343

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                TY  - JOUR
                AU  - Selnø, Anette Teo Hansen 
                AU  - Schlichtner, Stephanie 
                AU  - Yasinska, Inna M. 
                AU  - Sakhnevych, Svetlana S. 
                AU  - Fiedler, Walter 
                AU  - Wellbrock, Jasmin 
                AU  - Klenova, Elena 
                AU  - Pavlova, Ludmila 
                AU  - Gibbs, Bernhard F. 
                AU  - Degen, Martin 
                AU  - Schnyder, Isabelle 
                AU  - Aliu, Nijas 
                AU  - Berger, Steffen M. 
                AU  - Fasler-Kan, Elizaveta 
                AU  - Sumbayev, Vadim V. 
                TI  - Transforming growth factor beta type 1 (TGF-β) and hypoxia-inducible factor 1 (HIF-1) transcription complex as master regulators of the immunosuppressive protein galectin-9 expression in human cancer and embryonic cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202343
                DO  - 10.18632/aging.202343
                SP  - 23478
                EP  - 23496
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Selnø, Anette Teo Hansen 
                AU  - Schlichtner, Stephanie 
                AU  - Yasinska, Inna M. 
                AU  - Sakhnevych, Svetlana S. 
                AU  - Fiedler, Walter 
                AU  - Wellbrock, Jasmin 
                AU  - Klenova, Elena 
                AU  - Pavlova, Ludmila 
                AU  - Gibbs, Bernhard F. 
                AU  - Degen, Martin 
                AU  - Schnyder, Isabelle 
                AU  - Aliu, Nijas 
                AU  - Berger, Steffen M. 
                AU  - Fasler-Kan, Elizaveta 
                AU  - Sumbayev, Vadim V. 
                TI  - Transforming growth factor beta type 1 (TGF-β) and hypoxia-inducible factor 1 (HIF-1) transcription complex as master regulators of the immunosuppressive protein galectin-9 expression in human cancer and embryonic cells
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202343
                DO  - 10.18632/aging.202343
                SP  - 23478
                EP  - 23496
                PY  - 
                AB  - Galectin-9 is one of the key proteins employed by a variety of human malignancies to suppress anti-cancer activities of cytotoxic lymphoid cells and thus escape immune surveillance. Human cancer cells in most cases express higher levels of galectin-9 compared to non-transformed cells. However, the biochemical mechanisms underlying this phenomenon remain unclear.
                Here we report for the first time that in human cancer as well as embryonic cells, the transcription factors hypoxia-inducible factor 1 (HIF-1) and activator protein 1 (AP-1) are involved in upregulation of transforming growth factor beta 1 (TGF-&#x3B2;1) expression, leading to activation of the transcription factor Smad3 through autocrine action. This process triggers upregulation of galectin-9 expression in both malignant (mainly in breast and colorectal cancer as well as acute myeloid leukaemia (AML)) and embryonic cells. The effect, however, was not observed in mature non-transformed human cells. TGF-&#x3B2;1-activated Smad3 therefore displays differential behaviour in human cancer and embryonic vs non-malignant cells. This study uncovered a self-supporting biochemical mechanism underlying high levels of galectin-9 expression operated by the human cancer and embryonic cells employed in our investigations. Our results suggest the possibility of using the TGF-&#x3B2;1 signalling pathway as a potential highly efficient target for cancer immunotherapy.
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Pharmacological blockade of TNFα prevents sarcopenia and prolongs survival in aging mice

Clara Sciorati, Riccardo Gamberale, Antonella Monno, Lorena Citterio, Chiara Lanzani, Rebecca De Lorenzo, Giuseppe A. Ramirez, Antonio Esposito, Paolo Manunta, Angelo A. Manfredi, Patrizia Rovere-Querini,

https://doi.org/10.18632/aging.202200 pp 23497—23508

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Sciorati C, Gamberale R, Monno A, Citterio L, Lanzani C, De Lorenzo R, Ramirez GA, Esposito A, Manunta P, Manfredi AA, Rovere-Querini P, . Pharmacological blockade of TNFα prevents sarcopenia and prolongs survival in aging mice. . 12:23497-23508. https://doi.org/10.18632/aging.202200

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                TY  - JOUR
                AU  - Sciorati, Clara 
                AU  - Gamberale, Riccardo 
                AU  - Monno, Antonella 
                AU  - Citterio, Lorena 
                AU  - Lanzani, Chiara 
                AU  - De Lorenzo, Rebecca 
                AU  - Ramirez, Giuseppe A. 
                AU  - Esposito, Antonio 
                AU  - Manunta, Paolo 
                AU  - Manfredi, Angelo A. 
                AU  - Rovere-Querini, Patrizia 
                TI  - Pharmacological blockade of TNFα prevents sarcopenia and prolongs survival in aging mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202200
                DO  - 10.18632/aging.202200
                SP  - 23497
                EP  - 23508
                PY  - 
                AB  - Sarcopenia is a hallmark of aging. Inflammation due to increased generation of cytokines such as TNF&#x3B1;, IL-1&#x3B2; and IL-6 has been implicated in the pathogenesis of sarcopenia. In skeletal muscle of C57BL/6 mice from 12 until 28 months of age, we observed a progressive reduction of myofiber cross sectional area, loss of type II fibers and infiltration by inflammatory cells. Muscle strength decreased in parallel. Pharmacological TNF&#x3B1; blockade by weekly subcutaneous injection of Etanercept from 16 to 28 months of age prevented atrophy and loss of type II fibers, with significant improvements in muscle function and mice lifespan. The effects on leukocyte recruitment were limited. These results provide a proof of principle that endogenous TNF&#x3B1; is sufficient to cause sarcopenia and to reduce animal survival, and open a novel perspective on novel potential pharmacological treatment strategies based on TNF&#x3B1; blockade to prevent the noxious events associated with aging.
                ER  -

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FOXO3 longevity genotype mitigates the increased mortality risk in men with a cardiometabolic disease

Randi Chen, Brian J. Morris, Timothy A. Donlon, Kamal H. Masaki, D. Craig Willcox, Philip M.C. Davy, Richard C. Allsopp, Bradley J. Willcox,

https://doi.org/10.18632/aging.202175 pp 23509—23524

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Chen R, Morris BJ, Donlon TA, Masaki KH, Willcox DC, Davy PM, Allsopp RC, Willcox BJ, . FOXO3 longevity genotype mitigates the increased mortality risk in men with a cardiometabolic disease. . 12:23509-23524. https://doi.org/10.18632/aging.202175

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Provider: 
 TY - JOUR
 AU - Chen, Randi 
 AU - Morris, Brian J. 
 AU - Donlon, Timothy A. 
 AU - Masaki, Kamal H. 
 AU - Willcox, D. Craig 
 AU - Davy, Philip M.C. 
 AU - Allsopp, Richard C. 
 AU - Willcox, Bradley J. 
 TI - FOXO3 longevity genotype mitigates the increased mortality risk in men with a cardiometabolic disease
 JO - 
 JA - 
 VL - 12
 IS - 23
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.202175
 DO - 10.18632/aging.202175
 SP - 23509
 EP - 23524
 PY - 
 AB - FOXO3 is a prominent longevity gene. To date, no-one has examined whether longevity-associated FOXO3 genetic variants protect against mortality in all individuals, or only in those with aging-related diseases. We therefore tested longevity-associated FOXO3 single nucleotide polymorphisms in a haplotype block for association with mortality in 3,584 elderly American men of Japanese ancestry, 2,512 with and 1,072 without a cardiometabolic disease (CMD). At baseline (1991&#x2013;1993), 1,010 CMD subjects had diabetes, 1,919 had hypertension, and 738 had coronary heart disease (CHD). Follow-up until Dec 31, 2019 found that in CMD-affected individuals, longevity-associated alleles of FOXO3 were associated with significantly longer lifespan: haplotype hazard ratio 0.81 (95% CI 0.72-0.91; diabetes 0.77, hypertension 0.82, CHD 0.83). Overall, men with a CMD had higher mortality than men without a CMD (P=6x10-7). However, those men with a CMD who had the FOXO3 longevity genotype had similar survival as men without a CMD. In men without a CMD there was no association of longevity-associated alleles of FOXO3 with lifespan. Our study provides novel insights into the basis for the long-established role of FOXO3 as a longevity gene. We suggest that the FOXO3 longevity genotype increases lifespan only in at-risk individuals by protection against cardiometabolic stress.
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Mutation in histone deacetylase HDA-3 leads to shortened locomotor healthspan in Caenorhabditis elegans

Kazuto Kawamura, Ichiro N. Maruyama,

https://doi.org/10.18632/aging.202296 pp 23525—23547

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Kawamura K, Maruyama IN, . Mutation in histone deacetylase HDA-3 leads to shortened locomotor healthspan in Caenorhabditis elegans. . 12:23525-23547. https://doi.org/10.18632/aging.202296

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 TY - JOUR
 AU - Kawamura, Kazuto 
 AU - Maruyama, Ichiro N. 
 TI - Mutation in histone deacetylase HDA-3 leads to shortened locomotor healthspan in Caenorhabditis elegans
 JO - 
 JA - 
 VL - 12
 IS - 23
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.202296
 DO - 10.18632/aging.202296
 SP - 23525
 EP - 23547
 PY - 
 AB - Some genes are essential for survival, while other genes play modulatory roles on health and survival. Genes that play modulatory roles may promote an organism&#x2019;s survival and health by fine-tuning physiological processes. An unbiased search for genes that alter an organism&#x2019;s ability to maintain aspects of health may uncover modulators of lifespan and healthspan. From an unbiased screen for Caenorhabditis elegans mutants that show a progressive decline in motility, we aimed to identify genes that play a modulatory role in maintenance of locomotor healthspan. Here we report the involvement of hda-3, encoding a class I histone deacetylase, as a genetic factor that contributes in the maintenance of general health and locomotion in C. elegans. We identified a missense mutation in HDA-3 as the causative mutation in one of the isolated strains that show a progressive decline in maximum velocity and travel distance. From transcriptome analysis, we found a cluster of genes on Chromosome II carrying BATH domains that were downregulated by hda-3. Furthermore, downregulation of individual bath genes leads to significant decline in motility. Our study identifies genetic factors that modulate the maintenance of locomotor healthspan and may reveal potential targets for delaying age-related locomotor decline.
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PsychoAge and SubjAge: development of deep markers of psychological and subjective age using artificial intelligence

Alex Zhavoronkov, Kirill Kochetov, Peter Diamandis, Maria Mitina,

https://doi.org/10.18632/aging.202344 pp 23548—23577

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Zhavoronkov A, Kochetov K, Diamandis P, Mitina M, . PsychoAge and SubjAge: development of deep markers of psychological and subjective age using artificial intelligence. . 12:23548-23577. https://doi.org/10.18632/aging.202344

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                TY  - JOUR
                AU  - Zhavoronkov, Alex 
                AU  - Kochetov, Kirill 
                AU  - Diamandis, Peter 
                AU  - Mitina, Maria 
                TI  - PsychoAge and SubjAge: development of deep markers of psychological and subjective age using artificial intelligence
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202344
                DO  - 10.18632/aging.202344
                SP  - 23548
                EP  - 23577
                PY  - 
                AB  - Aging clocks that accurately predict human age based on various biodata types are among the most important recent advances in biogerontology. Since 2016 multiple deep learning solutions have been created to interpret facial photos, omics data, and clinical blood parameters in the context of aging. Some of them have been patented to be used in commercial settings. However, psychological changes occurring throughout the human lifespan have been overlooked in the field of &#x201C;deep aging clocks&#x201D;.
                In this paper, we present two deep learning predictors trained on social and behavioral data from Midlife in the United States (MIDUS) study: (a) PsychoAge, which predicts chronological age, and (b) SubjAge, which describes personal aging rate perception. Using 50 distinct features from the MIDUS dataset these models have achieved a mean absolute error of 6.7 years for chronological age and 7.3 years for subjective age. We also show that both PsychoAge and SubjAge are predictive of all-cause mortality risk, with SubjAge being a more significant risk factor.
                Both clocks contain actionable features that can be modified using social and behavioral interventions, which enables a variety of aging-related psychology experiment designs. The features used in these clocks are interpretable by human experts and may prove to be useful in shifting personal perception of aging towards a mindset that promotes productive and healthy behaviors.
                ER  -

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Leaky severe combined immunodeficiency in mice lacking non-homologous end joining factors XLF and MRI

Sergio Castañeda-Zegarra, Qindong Zhang, Amin Alirezaylavasani, Marion Fernandez-Berrocal, Rouan Yao, Valentyn Oksenych,

https://doi.org/10.18632/aging.202346 pp 23578—23597

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Castañeda-Zegarra S, Zhang Q, Alirezaylavasani A, Fernandez-Berrocal M, Yao R, Oksenych V, . Leaky severe combined immunodeficiency in mice lacking non-homologous end joining factors XLF and MRI. . 12:23578-23597. https://doi.org/10.18632/aging.202346

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                TY  - JOUR
                AU  - Castañeda-Zegarra, Sergio 
                AU  - Zhang, Qindong 
                AU  - Alirezaylavasani, Amin 
                AU  - Fernandez-Berrocal, Marion 
                AU  - Yao, Rouan 
                AU  - Oksenych, Valentyn 
                TI  - Leaky severe combined immunodeficiency in mice lacking non-homologous end joining factors XLF and MRI
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202346
                DO  - 10.18632/aging.202346
                SP  - 23578
                EP  - 23597
                PY  - 
                AB  - Non-homologous end-joining (NHEJ) is a DNA repair pathway required to detect, process, and ligate DNA double-stranded breaks (DSBs) throughout the cell cycle. The NHEJ pathway is necessary for V(D)J recombination in developing B and T lymphocytes. During NHEJ, Ku70 and Ku80 form a heterodimer that recognizes DSBs and promotes recruitment and function of downstream factors PAXX, MRI, DNA-PKcs, Artemis, XLF, XRCC4, and LIG4. Mutations in several known NHEJ genes result in severe combined immunodeficiency (SCID). Inactivation of Mri, Paxx or Xlf in mice results in normal or mild phenotype, while combined inactivation of Xlf/Mri, Xlf/Paxx, or Xlf/Dna-pkcs leads to late embryonic lethality. Here, we describe three new mouse models. We demonstrate that deletion of Trp53 rescues embryonic lethality in mice with combined deficiencies of Xlf and Mri. Furthermore, Xlf-/-Mri-/-Trp53+/- and Xlf-/-Paxx-/-Trp53+/- mice possess reduced body weight, severely reduced mature lymphocyte counts, and accumulation of progenitor B cells. We also report that combined inactivation of Mri/Paxx results in live-born mice with modest phenotype, and combined inactivation of Mri/Dna-pkcs results in embryonic lethality. Therefore, we conclude that XLF is functionally redundant with MRI and PAXX during lymphocyte development in vivo. Moreover, Mri genetically interacts with Dna-pkcs and Paxx.
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Exosome-mediated Hic-5 regulates proliferation and apoptosis of osteosarcoma via Wnt/β-catenin signal pathway

Liansheng Sha, Deying Ma, Cuili Chen,

https://doi.org/10.18632/aging.103546 pp 23598—23608

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Sha L, Ma D, Chen C, . Exosome-mediated Hic-5 regulates proliferation and apoptosis of osteosarcoma via Wnt/β-catenin signal pathway. . 12:23598-23608. https://doi.org/10.18632/aging.103546

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                TY  - JOUR
                AU  - Sha, Liansheng 
                AU  - Ma, Deying 
                AU  - Chen, Cuili 
                TI  - Exosome-mediated Hic-5 regulates proliferation and apoptosis of osteosarcoma via Wnt/β-catenin signal pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103546
                DO  - 10.18632/aging.103546
                SP  - 23598
                EP  - 23608
                PY  - 
                AB  - The expression of Hic-5 was detected in osteosarcoma patients and osteosarcoma cell lines by RT-PCR. Then RFP-sh-Hic-5 was transfected into osteosarcoma cell lines. The effect of Hic-5 on cell viability, proliferation and apoptosis were assessed by MTT, EdU kit and Flow cytometry. The exosomes were isolated from MG-63 cell supernatant by an Exosome Isolation Kit. The exosome-Hic-5 was confirmed by transmission electron microscope, particle size detection and RT-PCR. Next, exosome-Hic-5 treated cells were explored the cell viability, proliferation and apoptosis. Further, Co-IP assay was employed for identifying the relationship between Hic-5 and smad4. TCF/LEF and the protein level of components of wnt/&#x3B2;-catenin signals were detected by TOP luciferase assay and western blot. Hic-5 was upregulated in osteosarcoma tissues and cell. Forced decreased expression Hic-5 inhibited the proliferation of osteosarcoma cell lines, and induced apoptosis of MG-63 and HOS. In vivo, silencing Hic-5 remitted the tumor progression. Further, we isolated the exosomes from MG-63 supernatant, exosomes concluding Hic-5 would regulated the proliferation and apoptosis level of MG-63 and HOS cells. Further, Hic-5 interacted with smad4 and regulated Wnt/&#x3B2;-catenin signal by decreasing TCF/LEF activity. Silencing Hic-5 inhibited the proliferation and induced apoptosis of osteosarcoma cell via inactivating Wnt/&#x3B2;-catenin signal by exosome pathway.
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Inhibition of Exo-miR-19a-3p derived from cardiomyocytes promotes angiogenesis and improves heart function in mice with myocardial infarction via targeting HIF-1α

Lianping Gou, Cheng Xue, Xiaoyan Tang, Zhiyuan Fang,

https://doi.org/10.18632/aging.103563 pp 23609—23618

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Gou L, Xue C, Tang X, Fang Z, . Inhibition of Exo-miR-19a-3p derived from cardiomyocytes promotes angiogenesis and improves heart function in mice with myocardial infarction via targeting HIF-1α. . 12:23609-23618. https://doi.org/10.18632/aging.103563

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                TY  - JOUR
                AU  - Gou, Lianping 
                AU  - Xue, Cheng 
                AU  - Tang, Xiaoyan 
                AU  - Fang, Zhiyuan 
                TI  - Inhibition of Exo-miR-19a-3p derived from cardiomyocytes promotes angiogenesis and improves heart function in mice with myocardial infarction via targeting HIF-1α
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103563
                DO  - 10.18632/aging.103563
                SP  - 23609
                EP  - 23618
                PY  - 
                AB  - Background: Myocardial infarction (MI), a common presentation for cardiovascular disease, is caused by reduction of blood flow and oxygen supply and is one of the main causes of death worldwide. MicroRNAs participate in multiple physiological and pathological processed and play crucial role in myocardial infarction.
                Results: qRT-PCR analysis showed that expression level of miR-19a-3p was increased in serum of patient with MI. In vitro study indicated that the miR-19a-3p level was upregulated in response to H2O2 treatment and transferred by exosome, and then, uptake occurred in endothelial cells. Furthermore, western blot and immunostaining showed that treatment of exosome enriched miR-19a-3p suppressed the proliferation of endothelial cells and induced cell death, which was inhibited by AMO-19 transfection. Administration of antagomiR-19a-3p promoted angiogenesis and improved heart function of MI mice. Moreover, miR-19a-3p overexpression downregulated the protein level of HIF-1&#x3B1; and transfection of si-HIF-1&#x3B1; reversed the promotion of endothelial cells proliferation caused by AMO-19 transfection. In addition, antagomiR-19a-3p treatment accelerated angiogenesis and infection of AAV5-shHIF-1&#x3B1; inhibited that effect in MI mice.
                Conclusions: In conclusion, our finding indicated that miR-19a-3p inhibited endothelial cells proliferation and angiogenesis via targeting HIF-1&#x3B1; and attenuated heart function of mice after MI, and suggested a new mechanism of cell-to-cell communication between cardiomyocytes and endothelial cells.
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Pathomechanism characterization and potential therapeutics identification for SCA3 targeting neuroinflammation

Ya-Jen Chiu, Shu-An Lin, Wan-Ling Chen, Te-Hsien Lin, Chih-Hsin Lin, Ching-Fa Yao, Wenwei Lin, Yih-Ru Wu, Kuo-Hsuan Chang, Guey-Jen Lee-Chen, Chiung-Mei Chen,

https://doi.org/10.18632/aging.103700 pp 23619—23646

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Chiu Y, Lin S, Chen W, Lin T, Lin C, Yao C, Lin W, Wu Y, Chang K, Lee-Chen G, Chen C, . Pathomechanism characterization and potential therapeutics identification for SCA3 targeting neuroinflammation. . 12:23619-23646. https://doi.org/10.18632/aging.103700

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                TY  - JOUR
                AU  - Chiu, Ya-Jen 
                AU  - Lin, Shu-An 
                AU  - Chen, Wan-Ling 
                AU  - Lin, Te-Hsien 
                AU  - Lin, Chih-Hsin 
                AU  - Yao, Ching-Fa 
                AU  - Lin, Wenwei 
                AU  - Wu, Yih-Ru 
                AU  - Chang, Kuo-Hsuan 
                AU  - Lee-Chen, Guey-Jen 
                AU  - Chen, Chiung-Mei 
                TI  - Pathomechanism characterization and potential therapeutics identification for SCA3 targeting neuroinflammation
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103700
                DO  - 10.18632/aging.103700
                SP  - 23619
                EP  - 23646
                PY  - 
                AB  - Polyglutamine (polyQ)-mediated spinocerebellar ataxias (SCA) are caused by mutant genes with expanded CAG repeats encoding polyQ tracts. The misfolding and aggregation of polyQ proteins result in increased reactive oxygen species (ROS) and cellular toxicity. Inflammation is a common manifestation of oxidative stress and inflammatory process further reduces cellular antioxidant capacity. Increase of activated microglia in the pons of SCA type 3 (SCA3) patients suggests the involvement of neuroinflammation in the disease pathogenesis. In this study, we evaluated the anti-inflammatory potentials of indole compound NC009-1, 4-aminophenol-arachidonic acid derivative AM404, quinoline compound VB-037 and chalcone-coumarin derivative LM-031 using human HMC3 microglia and SCA3 ATXN3/Q75-GFP SH-SY5Y cells. The four tested compounds displayed anti-inflammatory activity by suppressing NO, IL-1&#x3B2;, TNF-&#x3B1; and IL-6 production and CD68 expression of IFN-&#x3B3;-activated HMC3 microglia. In retinoic acid-differentiated ATXN3/Q75-GFP SH-SY5Y cells inflamed with IFN-&#x3B3;-primed HMC3 conditioned medium, treatment with the tested compounds mitigated the increased caspase 1 activity and lactate dehydrogenase release, reduced polyQ aggregation and ROS and/or promoted neurite outgrowth. Examination of IL-1&#x3B2;- and TNF-&#x3B1;-mediated signaling pathways revealed that the tested compounds decreased I&#x3BA;B&#x3B1;/P65, JNK/JUN and/or P38/STAT1 signaling. The study results suggest the potential of NC009-1, AM404, VB-037 and LM-031 in treating SCA3 and probable other polyQ diseases.
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Identification of the novel Np17 oncogene in human leukemia

Bowen Wu, Yichao Gan, Ying Xu, Zhaoxing Wu, Ganyu Xu, Ping Wang, Chen Wang, Zhipeng Meng, Mengyuan Li, Jiawei Zhang, Haifeng Zhuang, Xuzhao Zhang, Linlin Yang, Jinfan Li, Xiaoxian Gan, Xiaofang Yu, Wendong Huang, Ying Gu, Rongzhen Xu,

https://doi.org/10.18632/aging.103808 pp 23647—23667

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Wu B, Gan Y, Xu Y, Wu Z, Xu G, Wang P, Wang C, Meng Z, Li M, Zhang J, Zhuang H, Zhang X, Yang L, et al, . Identification of the novel Np17 oncogene in human leukemia. . 12:23647-23667. https://doi.org/10.18632/aging.103808

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                TY  - JOUR
                AU  - Wu, Bowen 
                AU  - Gan, Yichao 
                AU  - Xu, Ying 
                AU  - Wu, Zhaoxing 
                AU  - Xu, Ganyu 
                AU  - Wang, Ping 
                AU  - Wang, Chen 
                AU  - Meng, Zhipeng 
                AU  - Li, Mengyuan 
                AU  - Zhang, Jiawei 
                AU  - Zhuang, Haifeng 
                AU  - Zhang, Xuzhao 
                AU  - Yang, Linlin 
                AU  - Li, Jinfan 
                AU  - Gan, Xiaoxian 
                AU  - Yu, Xiaofang 
                AU  - Huang, Wendong 
                AU  - Gu, Ying 
                AU  - Xu, Rongzhen 
                TI  - Identification of the novel Np17 oncogene in human leukemia
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103808
                DO  - 10.18632/aging.103808
                SP  - 23647
                EP  - 23667
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Wu, Bowen 
                AU  - Gan, Yichao 
                AU  - Xu, Ying 
                AU  - Wu, Zhaoxing 
                AU  - Xu, Ganyu 
                AU  - Wang, Ping 
                AU  - Wang, Chen 
                AU  - Meng, Zhipeng 
                AU  - Li, Mengyuan 
                AU  - Zhang, Jiawei 
                AU  - Zhuang, Haifeng 
                AU  - Zhang, Xuzhao 
                AU  - Yang, Linlin 
                AU  - Li, Jinfan 
                AU  - Gan, Xiaoxian 
                AU  - Yu, Xiaofang 
                AU  - Huang, Wendong 
                AU  - Gu, Ying 
                AU  - Xu, Rongzhen 
                TI  - Identification of the novel Np17 oncogene in human leukemia
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103808
                DO  - 10.18632/aging.103808
                SP  - 23647
                EP  - 23667
                PY  - 
                AB  - We previously defined the HERV-K Np9 as a viral oncogene. Here we report the discovery of a novel oncogene, Np17, which is homologous to the viral Np9 gene and predominantly present in Hominoidea. Np17 is located on chromosome 8, consists of 7 exons, and encodes a 16.8kDa nuclear protein with149 amino-acid residue. Functionally, knockdown of Np17 induced growth inhibition of leukemia cells, whereas enforced expression of Np17 promoted growth of leukemia cells in vitro and in vivo. In human leukemia, Np17 was detected in 59.65% (34/57) of acute myeloid leukemia (AML) patients examined and associated with refractory/relapsed AML. Mechanistically, Np17 decreased p53 levels and its mechanism might be involved in recruiting nuclear MDM2 to p53 for ubiquitin-mediated degradation. These findings reveal that Np17 is a novel oncogene associated with refractory/relapsed leukemia.
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DNMT3B silencing suppresses migration and invasion by epigenetically promoting miR-34a in bladder cancer

Kai Xu, Binshen Chen, Bingkun Li, Chaoming Li, Yiming Zhang, Ning Jiang, Bin Lang,

https://doi.org/10.18632/aging.103820 pp 23668—23683

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Xu K, Chen B, Li B, Li C, Zhang Y, Jiang N, Lang B, . DNMT3B silencing suppresses migration and invasion by epigenetically promoting miR-34a in bladder cancer. . 12:23668-23683. https://doi.org/10.18632/aging.103820

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                TY  - JOUR
                AU  - Xu, Kai 
                AU  - Chen, Binshen 
                AU  - Li, Bingkun 
                AU  - Li, Chaoming 
                AU  - Zhang, Yiming 
                AU  - Jiang, Ning 
                AU  - Lang, Bin 
                TI  - DNMT3B silencing suppresses migration and invasion by epigenetically promoting miR-34a in bladder cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103820
                DO  - 10.18632/aging.103820
                SP  - 23668
                EP  - 23683
                PY  - 
                AB  - The role of DNA methyltransferase 3B (DNMT3B) in tumorigenesis and development has been widely recognized; however, the mechanism underlying its action remains unclear. Considering its function in de novo methylation, we aimed to investigate whether DNMT3B plays its role via microRNA (miR)-34a promoter methylation in bladder cancer. We found that DNMT3B expression was low in 10 bladder cancer tissues and high in 20 bladder cancer tissues. miR-34a expression was higher in bladder cancer tissues with low expression of DNMT3B than that in bladder cancer tissues with high expression of DNMT3B. The level of miR-34a was negatively correlated with the level of DNMT3B. The methylation ratio of the miR-34a promoter was positively correlated with the level of DNMT3B and negatively correlated with the level of miR-34a. DNMT3B knockdown increased the expression of miR-34a and the transcriptional activity of the miR-34a promoter, while decreasing miR-34a promoter methylation. DNMT3B knockdown inhibited migration and invasion, while decreasing the protein levels of hepatocyte nuclear factor 4 gamma and Notch1 which are downstream targets of miR-34a. These inhibitory effects of DNMT3B were mitigated by the miR-34a inhibitor. In conclusion, DNMT3B silencing suppresses migration and invasion by epigenetically promoting miR-34a in bladder cancer.
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Hypoxia induces pulmonary artery smooth muscle dysfunction through mitochondrial fragmentation-mediated endoplasmic reticulum stress

Bing Zhuan, Xi Wang, Ming-Deng Wang, Zhi-Cai Li, Qun Yuan, Jun Xie, Zhao Yang,

https://doi.org/10.18632/aging.103892 pp 23684—23697

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Zhuan B, Wang X, Wang M, Li Z, Yuan Q, Xie J, Yang Z, . Hypoxia induces pulmonary artery smooth muscle dysfunction through mitochondrial fragmentation-mediated endoplasmic reticulum stress. . 12:23684-23697. https://doi.org/10.18632/aging.103892

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                TY  - JOUR
                AU  - Zhuan, Bing 
                AU  - Wang, Xi 
                AU  - Wang, Ming-Deng 
                AU  - Li, Zhi-Cai 
                AU  - Yuan, Qun 
                AU  - Xie, Jun 
                AU  - Yang, Zhao 
                TI  - Hypoxia induces pulmonary artery smooth muscle dysfunction through mitochondrial fragmentation-mediated endoplasmic reticulum stress
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103892
                DO  - 10.18632/aging.103892
                SP  - 23684
                EP  - 23697
                PY  - 
                AB  - Pulmonary arterial hypertension (PAH) is characterized by pulmonary artery smooth muscle cell (PASMC) dysfunction. However, the underlying mechanisms of PASMC dysfunction remain largely unknown. Here, we show that mitochondrial fragmentation contributes to PASMC dysfunction through enhancement of endoplasmic reticulum (ER) stress. PASMC dysfunction accompanied by mitochondrial fragmentation and ER stress was observed in the pulmonary arteries of hypoxia-induced rats with PAH, as well as isolated PASMCs under hypoxia. Treatment with Mdivi-1 inhibited mitochondrial fragmentation and ER stress and improved PASMC function in isolated PASMCs under hypoxia, while Drp1 overexpression increased mitochondrial fragmentation and ER stress, impairing PASMC function in isolated PASMCs under normoxia. However, inhibition of ER stress using ER stress inhibitors showed a negligible effect on mitochondrial morphology but improved PASMC function during hypoxia. Additionally, we found that mitochondrial fragmentation-promoted ER stress was dependent on mitochondrial reactive oxygen species. Furthermore, inhibition of mitochondrial fragmentation using Mdivi-1 attenuated mitochondrial fragmentation and ER stress in hypoxic PASMCs and improved the pulmonary artery smooth muscle function in hypoxic rats. These results suggest that hypoxia induces pulmonary artery smooth muscle dysfunction through mitochondrial fragmentation-mediated ER stress and that mitochondrial morphology is a potential target for treatment of hypoxia-induced pulmonary artery smooth muscle dysfunction.
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The ZiBuPiYin recipe regulates proteomic alterations in brain mitochondria-associated ER membranes caused by chronic psychological stress exposure: Implications for cognitive decline in Zucker diabetic fatty rats

Huiying Xu, Wen Zhou, Libin Zhan, Hua Sui, Lijing Zhang, Chunyan Zhao, Xiaoguang Lu,

https://doi.org/10.18632/aging.103894 pp 23698—23726

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Xu H, Zhou W, Zhan L, Sui H, Zhang L, Zhao C, Lu X, . The ZiBuPiYin recipe regulates proteomic alterations in brain mitochondria-associated ER membranes caused by chronic psychological stress exposure: Implications for cognitive decline in Zucker diabetic fatty rats. . 12:23698-23726. https://doi.org/10.18632/aging.103894

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                TY  - JOUR
                AU  - Xu, Huiying 
                AU  - Zhou, Wen 
                AU  - Zhan, Libin 
                AU  - Sui, Hua 
                AU  - Zhang, Lijing 
                AU  - Zhao, Chunyan 
                AU  - Lu, Xiaoguang 
                TI  - The ZiBuPiYin recipe regulates proteomic alterations in brain mitochondria-associated ER membranes caused by chronic psychological stress exposure: Implications for cognitive decline in Zucker diabetic fatty rats
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103894
                DO  - 10.18632/aging.103894
                SP  - 23698
                EP  - 23726
                PY  - 
                AB  - Chronic psychological stress (PS) cumulatively affects memory performance through the deleterious effects on hypothalamic-pituitary-adrenal axis regulation. Several functions damaged in cognitive impairment-related diseases are regulated by mitochondria-associated ER membranes (MAMs). To elucidate the role of ZiBuPiYin recipe (ZBPYR) in regulating the MAM proteome to improve PS-induced diabetes-associated cognitive decline (PSD), differentially expressed MAM proteins were identified among Zucker diabetic fatty rats, PSD rats, and PS combined with ZBPYR administration rats via iTRAQ with LC-MS/MS. Proteomic analysis revealed that the expressions of 85 and 33 proteins were altered by PS and ZBPYR treatment, respectively. Among these, 21 proteins were differentially expressed under both PS and ZBPYR treatments, whose functional categories included energy metabolism, lipid and protein metabolism, and synaptic dysfunction. Furthermore, calcium signaling and autophagy-related proteins may play roles in the pathogenesis of PSD and the mechanism of ZBPYR, respectively. Notably, KEGG pathway analysis suggested that &#x2018;Alzheimer&apos;s disease&#x2019; and &#x2018;oxidative phosphorylation&#x2019; pathways may be impaired in PSD pathogenesis, while ZBPYR could play a neuroprotective role through regulating the above pathways. Overall, exposure to chronic PS contributes to the evolution of diabetes-associated cognitive decline and ZBPYR might prevent and treat PSD by regulating the MAM proteome.
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Neurofilament light chain predicts risk of recurrence in cerebral amyloid angiopathy-related intracerebral hemorrhage

Xin Cheng, Ya Su, Qiong Wang, Feng Gao, Xiaofei Ye, Yiqing Wang, Yiwei Xia, Jiayu Fu, Yong Shen, Rustam Al-Shahi Salman, Qiang Dong,

https://doi.org/10.18632/aging.103927 pp 23727—23738

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Cheng X, Su Y, Wang Q, Gao F, Ye X, Wang Y, Xia Y, Fu J, Shen Y, Al-Shahi Salman R, Dong Q, . Neurofilament light chain predicts risk of recurrence in cerebral amyloid angiopathy-related intracerebral hemorrhage. . 12:23727-23738. https://doi.org/10.18632/aging.103927

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                TY  - JOUR
                AU  - Cheng, Xin 
                AU  - Su, Ya 
                AU  - Wang, Qiong 
                AU  - Gao, Feng 
                AU  - Ye, Xiaofei 
                AU  - Wang, Yiqing 
                AU  - Xia, Yiwei 
                AU  - Fu, Jiayu 
                AU  - Shen, Yong 
                AU  - Al-Shahi Salman, Rustam 
                AU  - Dong, Qiang 
                TI  - Neurofilament light chain predicts risk of recurrence in cerebral amyloid angiopathy-related intracerebral hemorrhage
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103927
                DO  - 10.18632/aging.103927
                SP  - 23727
                EP  - 23738
                PY  - 
                AB  - Predicting recurrent intracerebral hemorrhage (ICH) related to cerebral amyloid angiopathy (CAA) currently relies on brain images. We aimed to investigate whether blood neurodegenerative biomarkers predict disease severity and ICH recurrence in CAA. We recruited 68 first probable CAA-ICH cases from a Chinese prospective cohort, and 95 controls. We used the single-molecule array to measure acute phase blood amyloid-40, amyloid-42, total tau and neurofilament light chain (NfL). We used multivariable Cox regression models to assess the association between blood biomarkers and CAA-ICH recurrence, and used the concordance (c-) index to assess prediction models. Blood amyloid-42/40, total tau, and NfL levels changed in CAA-ICH cases than controls. During a median follow-up of 2.4 years, NfL was associated with CAA-ICH recurrence (adjusted hazard ratio 2.14, 95% CI 1.57-2.93) independent of MRI burden of small vessel disease (SVD). The performance of a model to predict CAA-ICH recurrence using MRI burden of SVD alone (c-index 0.77) increased with the addition of NfL (c-index 0.88, 95% CI 0.73-1.00, p=0.019). Further, NfL was associated with baseline ICH volume, NIHSS and 6-month mRS score. Blood NfL is associated with severity and prognosis of CAA-ICH and is a promising addition to MRI burden of SVD to predict CAA-ICH recurrence.
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Red light exaggerated sepsis-induced learning impairments and anxiety-like behaviors

Bing Xie, Yujing Zhang, Hong Qi, Hua Yao, You Shang, Shiying Yuan, Jiancheng Zhang,

https://doi.org/10.18632/aging.103940 pp 23739—23760

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Xie B, Zhang Y, Qi H, Yao H, Shang Y, Yuan S, Zhang J, . Red light exaggerated sepsis-induced learning impairments and anxiety-like behaviors. . 12:23739-23760. https://doi.org/10.18632/aging.103940

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                TY  - JOUR
                AU  - Xie, Bing 
                AU  - Zhang, Yujing 
                AU  - Qi, Hong 
                AU  - Yao, Hua 
                AU  - Shang, You 
                AU  - Yuan, Shiying 
                AU  - Zhang, Jiancheng 
                TI  - Red light exaggerated sepsis-induced learning impairments and anxiety-like behaviors
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103940
                DO  - 10.18632/aging.103940
                SP  - 23739
                EP  - 23760
                PY  - 
                AB  - Light exerts critical non-visual effects on a multitude of physiological processes and behaviors, including sleep-wake behavior and cognitive function. In this study, we investigated the effects of continued exposure to different colors of light on cognitive function after sepsis in old mice. We found that exposure to red light, but not green light, exaggerated learning impairments and anxiety-like behaviors after sepsis. Red light also induced remarkable splenomegaly and altered the diversity and composition of the fecal microbiota. Pseudo germ-free mice transplanted with fecal bacteria from septic mice exposed to red light developed the same behavioral defects and splenomegaly as their donors. Intriguingly, splenectomy and subdiaphragmatic vagotomy reversed the learning impairments and anxiety-like behaviors resulting from red light exposure after sepsis. After subdiaphragmatic vagotomy, no differences in behavior or spleen size were observed among pseudo germ-free mice transplanted with fecal bacteria from septic mice exposed to different colors of light. Our results suggested that red light exposure after sepsis in old mice causes gut microbiota dysfunction, thus stimulating signaling through the subdiaphragmatic vagus nerve that induces splenomegaly and aggravates learning impairments and anxiety-like behaviors.
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Serum KIAA1199 is an advanced-stage prognostic biomarker and metastatic oncogene in cholangiocarcinoma

Xiangyu Zhai, Wei Wang, Yunlong Ma, Yijia Zeng, Dandan Dou, Haoning Fan, Jianping Song, Xin Yu, Danqing Xin, Gang Du, Zhengchen Jiang, Hao Zhang, Xinlu Zhang, Bin Jin,

https://doi.org/10.18632/aging.103964 pp 23761—23777

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Zhai X, Wang W, Ma Y, Zeng Y, Dou D, Fan H, Song J, Yu X, Xin D, Du G, Jiang Z, Zhang H, Zhang X, et al, . Serum KIAA1199 is an advanced-stage prognostic biomarker and metastatic oncogene in cholangiocarcinoma. . 12:23761-23777. https://doi.org/10.18632/aging.103964

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                TY  - JOUR
                AU  - Zhai, Xiangyu 
                AU  - Wang, Wei 
                AU  - Ma, Yunlong 
                AU  - Zeng, Yijia 
                AU  - Dou, Dandan 
                AU  - Fan, Haoning 
                AU  - Song, Jianping 
                AU  - Yu, Xin 
                AU  - Xin, Danqing 
                AU  - Du, Gang 
                AU  - Jiang, Zhengchen 
                AU  - Zhang, Hao 
                AU  - Zhang, Xinlu 
                AU  - Jin, Bin 
                TI  - Serum KIAA1199 is an advanced-stage prognostic biomarker and metastatic oncogene in cholangiocarcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103964
                DO  - 10.18632/aging.103964
                SP  - 23761
                EP  - 23777
                PY  - 
                AB  - Background: Cell proliferation and migration are the determinants of malignant tumor progression, and a better understanding of related genes will lead to the identification of new targets aimed at preventing the spread of cancer. Some studies have shown that KIAA1199 (CEMIP) is a transmembrane protein expressed in many types of noncancerous cells and cancer cells. However, the potential role of KIAA1199 in the progression of cholangiocarcinoma (CCA) remains unclear.
                Results: Analysis of cancer-related databases showed that KIAA1199 is overexpressed in CCA. ELISA, immunohistochemistry, Western blotting and qPCR indicated high expression levels of KIAA1199 in serum, CCA tissues and CCA cell lines. In the serum (n = 41) and large sample validation (n = 177) cohorts, higher KIAA1199 expression was associated with shorter overall survival and disease-free survival times. At the cellular level, KIAA1199 overexpression (OE) promoted CCA growth and metastasis. Subcutaneous tumor xenograft experiments showed that KIAA1199 enhances CCA cell proliferation. Additionally, the expression levels of components in the EMT-related TGF-&#x3B2; pathway changed significantly after KIAA1199 upregulation and silencing.
                Conclusion: KIAA1199 is a promising new diagnostic molecule and therapeutic target in CCA. The serum KIAA1199 level can be used as a promising clinical tool for predicting the overall postoperative outcomes of patients with CCA.
                Methods: CCA-related KIAA1199 data were downloaded from the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases. To assess the prognostic impact of KIAA1199, an enzyme-linked immunosorbent assay (ELISA) was used to measure the serum level of KIAA1199 in 41 patients who underwent surgical resection. Immunohistochemical staining, Western blotting and qPCR were used to verify and retrospectively review the expression levels of KIAA1199 in cancer tissue specimens from 177 CCA patients. The effect of KIAA1199 on CCA was evaluated by cell-based functional assays and subcutaneous tumor xenograft experiments. The expression levels of proteins associated with epithelial-mesenchymal transition (EMT) and activation of relevant signaling pathways were measured via Western blotting.
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Colon cancer combined with obesity indicates improved survival- research on relevant mechanism

Zhou Yang, Xiyi Wei, Yitong Pan, Zhijun Min, Jingyuan Xu, Bo Yu,

https://doi.org/10.18632/aging.103972 pp 23778—23794

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Yang Z, Wei X, Pan Y, Min Z, Xu J, Yu B, . Colon cancer combined with obesity indicates improved survival- research on relevant mechanism. . 12:23778-23794. https://doi.org/10.18632/aging.103972

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                TY  - JOUR
                AU  - Yang, Zhou 
                AU  - Wei, Xiyi 
                AU  - Pan, Yitong 
                AU  - Min, Zhijun 
                AU  - Xu, Jingyuan 
                AU  - Yu, Bo 
                TI  - Colon cancer combined with obesity indicates improved survival- research on relevant mechanism
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103972
                DO  - 10.18632/aging.103972
                SP  - 23778
                EP  - 23794
                PY  - 
                AB  - Obesity contributes to the incidence of various tumors, including colon cancer. However, the impact of obesity on patients&#x2019; survival and related mechanisms remains unclear. Multi-omics data of 227 cases of colon cancer patients combined with clinical characteristics data were acquired from The Cancer Genome Atlas (TCGA) database. We confirmed obesity as an independent prognostic factor for improved overall survival of colon cancer patients. We demonstrated that hypoxia pathways were repressed in obese patients by regulating miR-210. Immune checkpoints PD-1 and LAG3 were also downregulated in obese patients, which indicated enhanced immune surveillance. The frequency of PIK3CA and KRAS mutations was decreased in obese patients. The sites and types of TP53 mutation were alternated in obesity patients. In conclusion, our research demonstrated the potential mechanisms of prolonged survival in colon cancer patients combined with obesity, which may provide potential value for improving the prognosis of colon cancer.
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Demethoxycurcumin analogue DMC-BH exhibits potent anticancer effects on orthotopic glioblastomas

Lei Shi, Guan Sun, Yong Zhang,

https://doi.org/10.18632/aging.103981 pp 23795—23807

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Shi L, Sun G, Zhang Y, . Demethoxycurcumin analogue DMC-BH exhibits potent anticancer effects on orthotopic glioblastomas. . 12:23795-23807. https://doi.org/10.18632/aging.103981

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                TY  - JOUR
                AU  - Shi, Lei 
                AU  - Sun, Guan 
                AU  - Zhang, Yong 
                TI  - Demethoxycurcumin analogue DMC-BH exhibits potent anticancer effects on orthotopic glioblastomas
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103981
                DO  - 10.18632/aging.103981
                SP  - 23795
                EP  - 23807
                PY  - 
                AB  - Demethoxycurcumin (DMC) has anti-glioma effects in vitro and in subcutaneous xenotransplanted tumors. Our previous study confirmed that the molecule also has mild anti-glioma effects on orthotopic glioblastomas in vivo. In this study, we found that DMC-BH, a DMC analogue, exhibited more potent in vitro and in vivo activities than did DMC. DMC-BH was cytotoxic against various glioma cells including SHG-44, C6, U251, U87, A172 and primary glioma cells. DMC-BH activity was characterized by low acute toxicity and an appropriate pharmacokinetic profile. We evaluated the anti-tumor effects of DMC-BH in an ectopic xenograft model, an orthotopic glioblastoma xenograft model and a patient-derived tumor xenograft (PDTX) model. DMC-BH exhibited potent anti-tumor activity in both the ectopic xenograft and PDTX models. Indeed, bioluminescence measurements showed that DMC-BH exerted a significantly greater anti-tumor effect on orthotopic glioma growth than DMC. Immunohistochemical analysis revealed that DMC-BH inhibited expression of Ki67 and increased the incidence of TUNEL-positive cells. Western blotting showed that DMC-BH significantly decreased p-Akt and p-mTOR expression in orthotopic glioma tissues. These results suggest that the DMC analogue DMC-BH has potent anti-tumor properties that warrant further study.
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Effect of Klotho protein during porcine oocyte maturation via Wnt signaling

Eui Hyun Kim, Anukul Taweechaipaisankul, Muhammad Rosyid Ridlo, Geon A Kim, Byeong Chun Lee,

https://doi.org/10.18632/aging.104002 pp 23808—23821

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Kim EH, Taweechaipaisankul A, Ridlo MR, Kim GA, Lee BC, . Effect of Klotho protein during porcine oocyte maturation via Wnt signaling. . 12:23808-23821. https://doi.org/10.18632/aging.104002

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                TY  - JOUR
                AU  - Kim, Eui Hyun 
                AU  - Taweechaipaisankul, Anukul 
                AU  - Ridlo, Muhammad Rosyid 
                AU  - Kim, Geon A 
                AU  - Lee, Byeong Chun 
                TI  - Effect of Klotho protein during porcine oocyte maturation via Wnt signaling
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104002
                DO  - 10.18632/aging.104002
                SP  - 23808
                EP  - 23821
                PY  - 
                AB  - Klotho protein is well-known as an anti-aging agent, however, several studies have suggested that Klotho protein also increases antioxidant activity and the reproductive system, as Klotho protein is closely associated with Wnt signaling. The objective of our study was to investigate the enhancement of porcine oocyte in vitro maturation via the Klotho protein-Wnt signaling pathway. Following immunohistochemistry and ELISA, we treated cells with Klotho protein during in vitro maturation. Lithium Chloride, a specific activator of Wnt signaling, was subsequently co-administered with Klotho protein. Mature oocytes subjected to treatments were used for the analysis of embryonic development, qRT-PCR, and immunocytochemistry. Treatment with 5pg/ml Klotho protein significantly increased cumulus cell expansion, blastocyst formation rates, and the total cell number of blastocysts. During cotreatment with 5mM Lithium Chloride and 5pg/ml Klotho protein, blastocyst formation rates were the highest in Klotho protein-treated oocytes and the lowest in Lithium Chloride-treated oocytes. Expression levels of Wnt signaling-related transcripts and proteins were significantly impacted by Klotho protein and Lithium Chloride. Moreover, cellular ATP levels and antioxidant activities were enhanced by Klotho protein treatment. These findings suggest a significant involvement of the Klotho protein-Wnt signaling mechanism in porcine oocyte maturation.
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Calreticulin increases growth and progression of natural killer/T-cell lymphoma

Yan Zheng, Chuntuan Li, Pengliang Xin, Qunyi Peng, Weiyu Zhang, Shengquan Liu, Xiongpeng Zhu,

https://doi.org/10.18632/aging.104030 pp 23822—23835

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Zheng Y, Li C, Xin P, Peng Q, Zhang W, Liu S, Zhu X, . Calreticulin increases growth and progression of natural killer/T-cell lymphoma. . 12:23822-23835. https://doi.org/10.18632/aging.104030

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                TY  - JOUR
                AU  - Zheng, Yan 
                AU  - Li, Chuntuan 
                AU  - Xin, Pengliang 
                AU  - Peng, Qunyi 
                AU  - Zhang, Weiyu 
                AU  - Liu, Shengquan 
                AU  - Zhu, Xiongpeng 
                TI  - Calreticulin increases growth and progression of natural killer/T-cell lymphoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104030
                DO  - 10.18632/aging.104030
                SP  - 23822
                EP  - 23835
                PY  - 
                AB  - In this study, we investigated the role of calreticulin (CALR) in the pathogenesis of natural killer/T-cell lymphoma (NKTCL). CALR expression was significantly higher in the NKTCL tissues than normal control tissues in the GSE80632 dataset. High CALR expression correlated with poorer overall survival of NKTCL patients (P = 0.0248). CALR mRNA and protein levels were significantly higher in NKTCL cell lines (NK92, SNK6, and SNT8) than normal NK cells. CALR-silenced SNK6 cells generated significantly smaller xenograft tumors in immunodeficient NCG mice than control SNK6 cells. CALR-knockdown NKTCL cells showed significantly less in vitro proliferation and Transwell migration than the controls. CALR knockdown inhibited G1-to-S phase cell cycle progression by increasing the levels of p27 cell cycle inhibitor and reducing the levels of cyclin E2 and cyclin-dependent kinase 2 (CDK2). CALR knockdown inhibited epithelial-to-mesenchymal transition (EMT) by decreasing the levels of &#x3B2;-catenin and TCF/ZEB1 and upregulating E-cadherin. These data demonstrate that CALR regulates the growth and progression of NKTCL cells by modulating G1-to-S cell cycle progression and EMT.
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Hsa_circ_0001869 promotes NSCLC progression via sponging miR-638 and enhancing FOSL2 expression

Pei Xu, Lei Wang, Xiao Xie, Fengqing Hu, Qi Yang, Rui Hu, Lianyong Jiang, Fangbao Ding, Ju Mei, Jianhui Liu, Haibo Xiao,

https://doi.org/10.18632/aging.104037 pp 23836—23848

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Xu P, Wang L, Xie X, Hu F, Yang Q, Hu R, Jiang L, Ding F, Mei J, Liu J, Xiao H, . Hsa_circ_0001869 promotes NSCLC progression via sponging miR-638 and enhancing FOSL2 expression. . 12:23836-23848. https://doi.org/10.18632/aging.104037

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                TY  - JOUR
                AU  - Xu, Pei 
                AU  - Wang, Lei 
                AU  - Xie, Xiao 
                AU  - Hu, Fengqing 
                AU  - Yang, Qi 
                AU  - Hu, Rui 
                AU  - Jiang, Lianyong 
                AU  - Ding, Fangbao 
                AU  - Mei, Ju 
                AU  - Liu, Jianhui 
                AU  - Xiao, Haibo 
                TI  - Hsa_circ_0001869 promotes NSCLC progression via sponging miR-638 and enhancing FOSL2 expression
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104037
                DO  - 10.18632/aging.104037
                SP  - 23836
                EP  - 23848
                PY  - 
                AB  - Accumulating studies suggest that circular RNAs (circRNAs) function as key regulators in human cancers. We found that hsa_circ_0001869 participated in non-small cell lung cancer (NSCLC) progression. However, its expression and function during NSCLC remain unknown. The data advised that hsa_circ_0001869 expression was increased in NSCLC cell lines and tissues. High hsa_circ_0001869 expression had negatively correlation with the NSCLC patients prognosis. Bioinformatics and luciferase report analyses confirmed that miR-638 and FOSL2 were hsa_circ_0001869 downstream target. hsa_circ_0001869 downregulation decreased tumor proliferation, invasion and migration by promoting miR-638 expression and decreasing FOSL2 expression. As a result of overexpression of FOSL2 or silencing of miR-638, the recovery of proliferation, migration, and invasion after hsa_circ_0001869 silencing. Overexpression of FOSL2 also led to recovery of migration, invasion and proliferation after upregulation of miR-638. In vivo studies confirmed that overexpression of FOSL2 or silencing of miR-638 led to the recovery of tumor growth ability regarding A549 cells after hsa_circ_0001869 knockdown. Present investigation discovered that hsa_circ_0001869 enhanced NSCLC progression via sponging miR-638 and promoting FOSL2 expression. hsa_circ_0001869 downregulation suppressed tumor growth and invasion ability.
                ER  -

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Integrative analysis reveals novel driver genes and molecular subclasses of hepatocellular carcinoma

Liguang Yang, Zhengtao Zhang, Yidi Sun, Shichao Pang, Qianlan Yao, Ping Lin, Jinming Cheng, Jia Li, Guohui Ding, Lijian Hui, Yixue Li, Hong Li,

https://doi.org/10.18632/aging.104047 pp 23849—23871

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Yang L, Zhang Z, Sun Y, Pang S, Yao Q, Lin P, Cheng J, Li J, Ding G, Hui L, Li Y, Li H, . Integrative analysis reveals novel driver genes and molecular subclasses of hepatocellular carcinoma. . 12:23849-23871. https://doi.org/10.18632/aging.104047

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                TY  - JOUR
                AU  - Yang, Liguang 
                AU  - Zhang, Zhengtao 
                AU  - Sun, Yidi 
                AU  - Pang, Shichao 
                AU  - Yao, Qianlan 
                AU  - Lin, Ping 
                AU  - Cheng, Jinming 
                AU  - Li, Jia 
                AU  - Ding, Guohui 
                AU  - Hui, Lijian 
                AU  - Li, Yixue 
                AU  - Li, Hong 
                TI  - Integrative analysis reveals novel driver genes and molecular subclasses of hepatocellular carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104047
                DO  - 10.18632/aging.104047
                SP  - 23849
                EP  - 23871
                PY  - 
                AB  - Hepatocellular carcinoma (HCC) is a heterogeneous disease with various genetic and epigenetic abnormalities. Previous studies of HCC driver genes were primarily based on frequency of mutations and copy number alterations. Here, we performed an integrative analysis of genomic and epigenomic data from 377 HCC patients to identify driver genes that regulate gene expression in HCC. This integrative approach has significant advantages over single-platform analyses for identifying cancer drivers. Using this approach, HCC tissues were divided into four subgroups, based on expression of the transcription factor E2F and the mutation status of TP53. HCC tissues with E2F overexpression and TP53 mutation had the highest cell cycle activity, indicating a synergistic effect of E2F and TP53. We found that overexpression of the identified driver genes, stratifin (SFN) and SPP1, correlates with tumor grade and poor survival in HCC and promotes HCC cell proliferation. These findings indicate SFN and SPP1 function as oncogenes in HCC and highlight the important role of enhancers in the regulation of gene expression in HCC.
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Apigenin-7-O-β-D-(-6”-p-coumaroyl)-glucopyranoside treatment elicits a neuroprotective effect through GSK-3β phosphorylation-mediated Nrf2 activation

Jingwen Wang, Shiquan Wang, Sisi Sun, Yunyang Lu, Kai Gao, Chao Guo, Ruili Li, Weiwei Li, Xian Zhao, Haifeng Tang, Aidong Wen, Min Cai, Wei Zhang,

https://doi.org/10.18632/aging.104050 pp 23872—23888

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Wang J, Wang S, Sun S, Lu Y, Gao K, Guo C, Li R, Li W, Zhao X, Tang H, Wen A, Cai M, Zhang W, . Apigenin-7-O-β-D-(-6”-p-coumaroyl)-glucopyranoside treatment elicits a neuroprotective effect through GSK-3β phosphorylation-mediated Nrf2 activation. . 12:23872-23888. https://doi.org/10.18632/aging.104050

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Provider: 
 TY - JOUR
 AU - Wang, Jingwen 
 AU - Wang, Shiquan 
 AU - Sun, Sisi 
 AU - Lu, Yunyang 
 AU - Gao, Kai 
 AU - Guo, Chao 
 AU - Li, Ruili 
 AU - Li, Weiwei 
 AU - Zhao, Xian 
 AU - Tang, Haifeng 
 AU - Wen, Aidong 
 AU - Cai, Min 
 AU - Zhang, Wei 
 TI - Apigenin-7-O-β-D-(-6”-p-coumaroyl)-glucopyranoside treatment elicits a neuroprotective effect through GSK-3β phosphorylation-mediated Nrf2 activation
 JO - 
 JA - 
 VL - 12
 IS - 23
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104050
 DO - 10.18632/aging.104050
 SP - 23872
 EP - 23888
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Wang, Jingwen 
 AU - Wang, Shiquan 
 AU - Sun, Sisi 
 AU - Lu, Yunyang 
 AU - Gao, Kai 
 AU - Guo, Chao 
 AU - Li, Ruili 
 AU - Li, Weiwei 
 AU - Zhao, Xian 
 AU - Tang, Haifeng 
 AU - Wen, Aidong 
 AU - Cai, Min 
 AU - Zhang, Wei 
 TI - Apigenin-7-O-β-D-(-6”-p-coumaroyl)-glucopyranoside treatment elicits a neuroprotective effect through GSK-3β phosphorylation-mediated Nrf2 activation
 JO - 
 JA - 
 VL - 12
 IS - 23
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104050
 DO - 10.18632/aging.104050
 SP - 23872
 EP - 23888
 PY - 
 AB - The current study was designed to seek the role of the glycogen synthase kinase-3&#x3B2; (GSK-&#x3B2;)-regulated NF-E2-related factor 2 (Nrf2) pathway in the antioxidant effect induced by Apigenin-7-O-&#x3B2;-D-(-6&#x201D;-p-coumaroyl)-glucopyranoside (APG). Rat primary cultured cortical neurons were challenged by oxygen and glucose deprivation/reoxygenation (OGD/R) and then treated with APG. Cell viability, phosphorylation of GSK-&#x3B2; at Ser9 and nuclear expression of Nrf2 were measured. Male Sprague Dawley rats challenged by 2-h middle cerebral artery occlusion were treated with 50 mg/kg APG, and the neurological score, infarct volume, phosphorylation of GSK-3&#x3B2; and nuclear expression of Nrf2 were analyzed. The neuroprotective effect of APG and the expression levels of antioxidant enzymes and oxidative products were also examined in the presence and absence of Nrf2-siRNA and PI3K inhibitors. APG reduced the apoptotic proportion, attenuated LDH release and increased cell viability, and in vivo, APG improved neurological scores and reduced infarct volume. APG increased GSK-3&#x3B2; phosphorylation and Nrf2 nuclear translocation, while these effects were prevented by PI3K inhibitors or Nrf2-siRNA treatment in both OGD/R cell cultures and ischemic/reperfusion rats. These findings reveal that GSK-3&#x3B2; phosphorylation-mediated Nrf2 activation is involved in the neuroprotective effect of APG.
 ER -

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Cohort profile: the Diet and Healthy Aging (DaHA) study in Singapore

Rongjun Yu, Ye Sun, Kaisy Xinhong Ye, Qiushi Feng, Su Lin Lim, Rathi Mahendran, Irwin Kee-Mun Cheah, Roger Sik Yin Foo, Ru Yuan Chua, Xinyi Gwee, Marie Loh, Rani Sarmugam, Wei Wei Thwe Khine, Yin Xia Chao, Anis Larbi, Yuan Kun Lee, Alan Prem Kumar, Brian K. Kennedy, Ee Heok Kua, Lei Feng,

https://doi.org/10.18632/aging.104051 pp 23889—23899

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Yu R, Sun Y, Ye KX, Feng Q, Lim SL, Mahendran R, Cheah IK, Foo RSY, Chua RY, Gwee X, Loh M, Sarmugam R, Khine WWT, et al, . Cohort profile: the Diet and Healthy Aging (DaHA) study in Singapore. . 12:23889-23899. https://doi.org/10.18632/aging.104051

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                TY  - JOUR
                AU  - Yu, Rongjun 
                AU  - Sun, Ye 
                AU  - Ye, Kaisy Xinhong 
                AU  - Feng, Qiushi 
                AU  - Lim, Su Lin 
                AU  - Mahendran, Rathi 
                AU  - Cheah, Irwin Kee-Mun 
                AU  - Foo, Roger Sik Yin 
                AU  - Chua, Ru Yuan 
                AU  - Gwee, Xinyi 
                AU  - Loh, Marie 
                AU  - Sarmugam, Rani 
                AU  - Khine, Wei Wei Thwe 
                AU  - Chao, Yin Xia 
                AU  - Larbi, Anis 
                AU  - Lee, Yuan Kun 
                AU  - Kumar, Alan Prem 
                AU  - Kennedy, Brian K. 
                AU  - Kua, Ee Heok 
                AU  - Feng, Lei 
                TI  - Cohort profile: the Diet and Healthy Aging (DaHA) study in Singapore
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104051
                DO  - 10.18632/aging.104051
                SP  - 23889
                EP  - 23899
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Yu, Rongjun 
                AU  - Sun, Ye 
                AU  - Ye, Kaisy Xinhong 
                AU  - Feng, Qiushi 
                AU  - Lim, Su Lin 
                AU  - Mahendran, Rathi 
                AU  - Cheah, Irwin Kee-Mun 
                AU  - Foo, Roger Sik Yin 
                AU  - Chua, Ru Yuan 
                AU  - Gwee, Xinyi 
                AU  - Loh, Marie 
                AU  - Sarmugam, Rani 
                AU  - Khine, Wei Wei Thwe 
                AU  - Chao, Yin Xia 
                AU  - Larbi, Anis 
                AU  - Lee, Yuan Kun 
                AU  - Kumar, Alan Prem 
                AU  - Kennedy, Brian K. 
                AU  - Kua, Ee Heok 
                AU  - Feng, Lei 
                TI  - Cohort profile: the Diet and Healthy Aging (DaHA) study in Singapore
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104051
                DO  - 10.18632/aging.104051
                SP  - 23889
                EP  - 23899
                PY  - 
                AB  - How diet is related with cognition and health has not been systematically examined in Asians whose eating habits are very different from their counterparts in the West and the biological mechanisms underlying such links are not well known yet. The diet and healthy aging (DaHA) study is a community-based longitudinal study conducted to examine the role of diet and nutrition in promoting cognitive, emotional, and physical health among community-living elderly Singaporeans. The first wave of DaHA, conducted from 2011 to 2017, provided detailed information on diet and baseline cognitive function and health from 1010 community-living elderly in Singapore. Biomarkers of oxidative stress, systemic inflammation, and genetic information were collected. The ongoing second wave of DaHA is conducted from 2017 to 2020, which provides follow- up assessments using established cognitive tests and clinical tools. This well-characterized cohort, with its archived biological samples and high-quality data on diet and lifestyle factors will allow researchers to explore the relationships among diet, nutrition, genes, cognition, mental and physical health in an extremely cost-effective manner. Translations of the research findings into clinical and public health practices will potentially help to promote cognitive health at the population level and reduce healthcare costs related to cognitive impairment.
                ER  -

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Female-specific effects of the catechol-O-methyl transferase Val¹⁵⁸Met gene polymorphism on working memory-related brain function

Jialing Fan, Caishui Yang, Zhen Liu, He Li, Yan Han, Kewei Chen, Chuansheng Chen, Jun Wang, Zhanjun Zhang,

https://doi.org/10.18632/aging.104059 pp 23900—23916

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Fan J, Yang C, Liu Z, Li H, Han Y, Chen K, Chen C, Wang J, Zhang Z, . Female-specific effects of the catechol-O-methyl transferase Val¹⁵⁸Met gene polymorphism on working memory-related brain function. . 12:23900-23916. https://doi.org/10.18632/aging.104059

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Provider: 
 TY - JOUR
 AU - Fan, Jialing 
 AU - Yang, Caishui 
 AU - Liu, Zhen 
 AU - Li, He 
 AU - Han, Yan 
 AU - Chen, Kewei 
 AU - Chen, Chuansheng 
 AU - Wang, Jun 
 AU - Zhang, Zhanjun 
 TI - Female-specific effects of the catechol-O-methyl transferase Val158Met gene polymorphism on working memory-related brain function
 JO - 
 JA - 
 VL - 12
 IS - 23
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.104059
 DO - 10.18632/aging.104059
 SP - 23900
 EP - 23916
 PY - 
 AB - The catechol-O-methyltransferase (COMT) Val158Met polymorphism has been associated with working memory (WM) in many studies, but the results have not been consistent. One plausible explanation is sex-specific effects of this polymorphism as reported in several studies. The current study aimed to explore the sex-specific effects of the COMT Val158Met polymorphism on WM-related brain function in an elderly sample. We found that Val homozygotes outperformed Met allele carriers on the backward digit span subtest for both males and females. The triangular part of the left inferior frontal gyrus and the left inferior temporal gyrus exhibited higher activation in Met allele carriers compared with Val homozygotes during the n-back task, while the background functional connectivity (bFC) between the left angular gyrus (ANG) and the right ANG was enhanced in Val homozygotes as compared to Met allele carriers. Finally, the associations between brain activation, bFC (among various regions), and WM performance were identified only in specific genotype groups of the female participants. These findings provide new insights into the role of COMT Val158Met gene polymorphism in brain function, particularly its female-specific nature.
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Molecular subtypes based on DNA promoter methylation predict prognosis in lung adenocarcinoma patients

Shanping Shi, Mingjun Xu, Yang Xi,

https://doi.org/10.18632/aging.104062 pp 23917—23930

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Shi S, Xu M, Xi Y, . Molecular subtypes based on DNA promoter methylation predict prognosis in lung adenocarcinoma patients. . 12:23917-23930. https://doi.org/10.18632/aging.104062

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                TY  - JOUR
                AU  - Shi, Shanping 
                AU  - Xu, Mingjun 
                AU  - Xi, Yang 
                TI  - Molecular subtypes based on DNA promoter methylation predict prognosis in lung adenocarcinoma patients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104062
                DO  - 10.18632/aging.104062
                SP  - 23917
                EP  - 23930
                PY  - 
                AB  - Background: The heterogeneity of lung adenocarcinoma (LADC) makes the early diagnosis and treatment of the disease difficult. Gene silencing of DNA methylation is an important mechanism of tumorigenesis. A combination of methylation and clinical features can improve the classification of LADC heterogeneity.
                Results: We investigated the prognostic significance of 335 specimen subgroups of Lung adenocarcinoma based on the DNA methylation level. The differences in DNA methylation levels were related to the TNM stage classification, age, gender, and prognostic values. Seven subtypes were determined using 774 CpG sites that significantly affected the survival rate based on the consensus clustering. Finally, we constructed a prognostic model that performed well and further verified it in our test group.
                Conclusions: This study shows that classification based on DNA methylation might aid in demonstrating heterogeneity within formerly characterized LADC molecular subtypes, assisting in the development of efficient, personalized therapy.
                Methods: Methylation data of lung adenocarcinoma were downloaded from the University of California Santa Cruz (UCSC) cancer browser, and the clinical patient information and RNA-seq archives were acquired from the Cancer Genome Atlas (TCGA). CpG sites were identified based on the significant correlation with the prognosis and used further to cluster the cases uniformly into several subtypes.
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Clinical and prognostic pan-cancer analysis of m6A RNA methylation regulators in four types of endocrine system tumors

Kai Li, Haiqing Luo, Hui Luo, Xiao Zhu,

https://doi.org/10.18632/aging.104064 pp 23931—23944

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Li K, Luo H, Luo H, Zhu X, . Clinical and prognostic pan-cancer analysis of m6A RNA methylation regulators in four types of endocrine system tumors. . 12:23931-23944. https://doi.org/10.18632/aging.104064

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                TY  - JOUR
                AU  - Li, Kai 
                AU  - Luo, Haiqing 
                AU  - Luo, Hui 
                AU  - Zhu, Xiao 
                TI  - Clinical and prognostic pan-cancer analysis of m6A RNA methylation regulators in four types of endocrine system tumors
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104064
                DO  - 10.18632/aging.104064
                SP  - 23931
                EP  - 23944
                PY  - 
                AB  - N6-methyladenosine (m6A), internal modification of mRNA, has recently been reported to be an important regulatory mechanism affecting tumor proliferation. However, its role in endocrine system tumors is poorly understood. We obtained datasets for four types tumors from the TCGA database, analyzed the GTEx database as a supplement to the control group, and used &#x201C;Perl&#x201D; and &#x201C;R&#x201D; software to analyze the datasets. Then we differentiated the expression level, used it to cluster consensus. Besides, we established lasso regression model to screen variables, used univariate and multivariate cox analyses to explore the independent risk factors associated with cancer prognosis. The results indicated that except for WTAP, the expression level of METTL3 was negatively correlated with other genes. The expression level of WTAP and METTL16 was positively correlated with overall survival (OS). Moreover, we found that different clinical subtypes of adrenal cortical carcinoma had significant differences in survival status, histologic grading, pathological T grade, and OS. Furthermore, different clinical subtypes of thyroid carcinoma had significant differences in histologic grading and pathological T grade. The differential expression of m6A regulatory genes is closely associated with the presence of endocrine-system-related tumors, and risk scores can be used to assess prognosis.
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In-depth transcriptomic analyses of LncRNA and mRNA expression in the hippocampus of APP/PS1 mice by Danggui-Shaoyao-San

Zhenyan Song, Fuzhou Li, Chunxiang He, Jingping Yu, Ping Li, Ze Li, Miao Yang, Shaowu Cheng,

https://doi.org/10.18632/aging.104068 pp 23945—23959

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Song Z, Li F, He C, Yu J, Li P, Li Z, Yang M, Cheng S, . In-depth transcriptomic analyses of LncRNA and mRNA expression in the hippocampus of APP/PS1 mice by Danggui-Shaoyao-San. . 12:23945-23959. https://doi.org/10.18632/aging.104068

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                TY  - JOUR
                AU  - Song, Zhenyan 
                AU  - Li, Fuzhou 
                AU  - He, Chunxiang 
                AU  - Yu, Jingping 
                AU  - Li, Ping 
                AU  - Li, Ze 
                AU  - Yang, Miao 
                AU  - Cheng, Shaowu 
                TI  - In-depth transcriptomic analyses of LncRNA and mRNA expression in the hippocampus of APP/PS1 mice by Danggui-Shaoyao-San
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104068
                DO  - 10.18632/aging.104068
                SP  - 23945
                EP  - 23959
                PY  - 
                AB  - Alzheimer&#x2019;s disease (AD) is an age-related neurodegenerative disease with a high incidence worldwide, and with no medications currently able to prevent the progression of AD. Danggui-Shaoyao-San (DSS) is widely used in traditional Chinese medicine (TCM) and has been proven to be effective for memory and cognitive dysfunction, yet its precise mechanism remains to be delineated. The present study was designed to investigate the genome-wide expression profile of long non-coding RNAs (LncRNAs) and messenger RNAs (mRNAs) in the hippocampus of APP/PS1 mice after DSS treatment by RNA sequencing. A total of 285 differentially expressed LncRNAs and 137 differentially expressed mRNAs were identified (fold-change &#x2265;2.0 and P &lt; 0.05). Partial differentially expressed LncRNAs and mRNAs were selected to verify the RNA sequencing results by quantitative polymerase chain reaction (qPCR). A co-expression network was established to analyze co-expressed LncRNAs and genes. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were used to evaluate the biological functions related to the differentially co-expressed LncRNAs, and the results showed that the co-expressed LncRNAs were mainly involved in AD development from distinct origins, such as APP processing, neuron migration, and synaptic transmission. Our research describes the lncRNA and mRNA expression profiles and functional networks involved in the therapeutic effect of DSS in APP/PS1 mice model. The results suggest that the therapeutic effect of DSS on AD involves the expression of LncRNAs. Our findings provide a new perspective for research on the treatment of complex diseases using traditional Chinese medicine prescriptions.
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The long noncoding RNA HCG18 participates in PM2.5-mediated vascular endothelial barrier dysfunction

Shiwen Wang, Yuyin Lin, Yue Zhong, Maozhou Zhao, Wei Yao, Xiaohui Ren, Qin Wang, Xiaolan Guo, Qian-Qian Zhang, Jianwei Dai,

https://doi.org/10.18632/aging.104073 pp 23960—23973

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Wang S, Lin Y, Zhong Y, Zhao M, Yao W, Ren X, Wang Q, Guo X, Zhang Q, Dai J, . The long noncoding RNA HCG18 participates in PM2.5-mediated vascular endothelial barrier dysfunction. . 12:23960-23973. https://doi.org/10.18632/aging.104073

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                TY  - JOUR
                AU  - Wang, Shiwen 
                AU  - Lin, Yuyin 
                AU  - Zhong, Yue 
                AU  - Zhao, Maozhou 
                AU  - Yao, Wei 
                AU  - Ren, Xiaohui 
                AU  - Wang, Qin 
                AU  - Guo, Xiaolan 
                AU  - Zhang, Qian-Qian 
                AU  - Dai, Jianwei 
                TI  - The long noncoding RNA HCG18 participates in PM2.5-mediated vascular endothelial barrier dysfunction
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104073
                DO  - 10.18632/aging.104073
                SP  - 23960
                EP  - 23973
                PY  - 
                AB  - Increased vascular endothelial permeability can disrupt vascular barrier function and further lead to multiple human diseases. Our previous reports indicated that particulate matter 2.5 (PM2.5) can enhance the permeability of vascular endothelial cells. However, the regulatory mechanism was not comprehensively demonstrated. Therefore, this work elucidated this mechanism by demonstrating that PM2.5 can increase the permeability of HUVECs by inhibiting the expression of Hickson compact group 18 (HCG18). Moreover, we demonstrated that lncRNA HCG18 functioned as a ceRNA for miR-21-5p and led to the derepression of its target SOX7, which could further transcriptionally activate the expression of VE-cadherin to regulate the permeability of HUVECs. In this study, we provide evidence that HCG18/miR-21-5p/SOX7/VE-cadherin signaling is involved in PM2.5-induced vascular endothelial barrier dysfunction.
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Effect of lncRNA WT1-AS regulating WT1 on oxidative stress injury and apoptosis of neurons in Alzheimer's disease via inhibition of the miR-375/SIX4 axis

Quanbao Wang, Xiumin Ge, Jie Zhang, Licheng Chen,

https://doi.org/10.18632/aging.104079 pp 23974—23995

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Wang Q, Ge X, Zhang J, Chen L, . Effect of lncRNA WT1-AS regulating WT1 on oxidative stress injury and apoptosis of neurons in Alzheimer's disease via inhibition of the miR-375/SIX4 axis. . 12:23974-23995. https://doi.org/10.18632/aging.104079

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                TY  - JOUR
                AU  - Wang, Quanbao 
                AU  - Ge, Xiumin 
                AU  - Zhang, Jie 
                AU  - Chen, Licheng 
                TI  - Effect of lncRNA WT1-AS regulating WT1 on oxidative stress injury and apoptosis of neurons in Alzheimer's disease via inhibition of the miR-375/SIX4 axis
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104079
                DO  - 10.18632/aging.104079
                SP  - 23974
                EP  - 23995
                PY  - 
                AB  - Objective: To study the effect of lncRNA WT1-AS on oxidative stress injury (OSI) and apoptosis of neurons in Alzheimer&apos;s disease (AD) and its specific mechanisms related to the microRNA-375 (miR-375)/SIX4 axis and WT1 expression.
                Results: After bioinformatic prediction, WT1-AS was found to be downregulated in A&#x3B2;25-35treated SH-SY5Y cells, and WT1-AS overexpression inhibited WT1 expression. WT1 could target miR-375 to promote its expression. miR-375 bound to SIX4, and miR-375 overexpression inhibited SIX4 expression. WT1-AS inhibited OSI and apoptosis, while WT1 and miR-375 overexpression or SIX4 silencing reversed the WT1-AS effect on OSI and apoptosis. In vivo experiments revealed that WT1-AS improved learning/memory abilities and inhibited OSI and apoptosis in AD mice.
                Conclusion: Overexpression of WT1-AS can inhibit the miR-375/SIX4 axis, OSI and neuronal apoptosis in AD by inhibiting WT1 expression.
                Methods: Related lncRNAs were identified, and miR-375 downstream targets were predicted. WT1-AS, WT1, miR-375 and SIX4 expression was detected in a cell model induced by A&#x3B2;25-35. The binding of WT1 with miR-375 and that of miR-375 with SIX4 were further confirmed. Adenosine triphosphate (ATP), reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and lactate dehydrogenase (LDH) activities, and apoptosis levels were tested after mitochondrial membrane potential observation. Learning/memory abilities and neuronal apoptosis were tested in a mouse model.
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Hsa_circ_0048179 attenuates free fatty acid-induced steatosis via hsa_circ_0048179/miR-188-3p/GPX4 signaling

Wenjun Yang, Jinduo Zhao, Ye Zhao, Wenfeng Li, Liang Zhao, Yi Ren, Rongying Ou, Yunsheng Xu,

https://doi.org/10.18632/aging.104081 pp 23996—24008

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Yang W, Zhao J, Zhao Y, Li W, Zhao L, Ren Y, Ou R, Xu Y, . Hsa_circ_0048179 attenuates free fatty acid-induced steatosis via hsa_circ_0048179/miR-188-3p/GPX4 signaling. . 12:23996-24008. https://doi.org/10.18632/aging.104081

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                TY  - JOUR
                AU  - Yang, Wenjun 
                AU  - Zhao, Jinduo 
                AU  - Zhao, Ye 
                AU  - Li, Wenfeng 
                AU  - Zhao, Liang 
                AU  - Ren, Yi 
                AU  - Ou, Rongying 
                AU  - Xu, Yunsheng 
                TI  - Hsa_circ_0048179 attenuates free fatty acid-induced steatosis via hsa_circ_0048179/miR-188-3p/GPX4 signaling
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104081
                DO  - 10.18632/aging.104081
                SP  - 23996
                EP  - 24008
                PY  - 
                AB  - Although circular RNAs (circRNAs) are known to play key roles in non-alcoholic fatty liver disease, much about their targets and mechanisms remains unknown. We therefore investigated the actions and mechanisms of hsa_circ_0048179 in an in vitro model of NAFLD. HepG2 cells were exposed to oleate/palmitate (2:1 ratio) for 24 h to induce intracellular lipid accumulation. Using CCK-8 assays, flow cytometry, fluorescence microscopy, western blotting, RT-qPCR, and Oil red O staining, we found that oleate/palmitate treatment reduced cell viability while increasing apoptosis and lipid accumulation in HepG2 cells. Levels of the antioxidant enzyme GPX4 were decreased in oleate/palmitate-treated HepG2 cells, and there were corresponding increases in reactive oxygen species and damage to mitochondrial cristae. Levels of hsa_circ_0048179 expression were also suppressed by oleate/palmitate treatment, and GPX4 levels were markedly increased in HepG2 cells following transfection with hsa_circ_0048179. Analysis of its mechanism revealed that hsa_circ_0048179 upregulated GPX4 levels by acting as a competitive &#x201C;sponge&#x201D; of miR-188-3p and that hsa_circ_0048179 attenuated oleate/palmitate-induced lipid accumulation in HepG2 cells by sponging miR-188-3p. Collectively, our findings suggest that hsa_circ_0048179 may play a key role in the pathogenesis of steatosis and may thus be a useful target for drug development.
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Extracellular vesicle derived miR-544 downregulates expression of tumor suppressor promyelocytic leukemia zinc finger resulting in increased peritoneal metastasis in gastric cancer

Wencheng Kong, Xinchun Liu, Guang Yin, Sixin Zheng, Akao Zhu, Panpan Yu, Yuqiang Shan, Rongchao Ying, Jian Zhang,

https://doi.org/10.18632/aging.104082 pp 24009—24022

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Kong W, Liu X, Yin G, Zheng S, Zhu A, Yu P, Shan Y, Ying R, Zhang J, . Extracellular vesicle derived miR-544 downregulates expression of tumor suppressor promyelocytic leukemia zinc finger resulting in increased peritoneal metastasis in gastric cancer. . 12:24009-24022. https://doi.org/10.18632/aging.104082

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                TY  - JOUR
                AU  - Kong, Wencheng 
                AU  - Liu, Xinchun 
                AU  - Yin, Guang 
                AU  - Zheng, Sixin 
                AU  - Zhu, Akao 
                AU  - Yu, Panpan 
                AU  - Shan, Yuqiang 
                AU  - Ying, Rongchao 
                AU  - Zhang, Jian 
                TI  - Extracellular vesicle derived miR-544 downregulates expression of tumor suppressor promyelocytic leukemia zinc finger resulting in increased peritoneal metastasis in gastric cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104082
                DO  - 10.18632/aging.104082
                SP  - 24009
                EP  - 24022
                PY  - 
                AB  - Peritoneal metastasis (PM) is the main cause of poor prognosis in patients with advanced gastric cancer (GC). Increasing evidence has suggested that cancer-associated EVs in body fluids may assist in the diagnosis and treatment of GC. Here, we investigated the role of GC-derived EVs in PM development. Our results demonstrate that expression of the tumor suppressor promyelocytic leukemia zinc finger (PLZF) is decreased in GC tissues and PM lesions from GC patients. PLZF suppression promoted migration and invasion of peritoneal mesothelial HMrSV5 cells, while PLZF overexpression suppressed HMrSV5 cell migration and invasion. Microarray analysis revealed significantly upregulated expression of several miRNAs in EVs isolated from GC patients with PM, including miR-544. The increased miR-544 expression was confirmed in GC tissues and PM-derived EVs. Transfection with miR-544 reduced PLZF expression in HMrSV5 cells, while miR-544 inhibition increased PLZF expression. Incubation of GC cells with peritoneal mesothelial HMrSV5 cells showed that miR-544 could be transferred from GC-derived EVs to peritoneal cells, where it suppressed the PLZF expression. These findings indicate that EV-mediated transfer of miR-544 decreases the PLZF expression in PM lesions, which suggests miR-544 could potentially serve as a diagnostic biomarker and therapeutic target for treatment of GC patients.
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Islet transplantation modulates macrophage to induce immune tolerance and angiogenesis of islet tissue in type I diabetes mice model

Yang Li, Xiaoming Ding, Xiaohui Tian, Jin Zheng, Chenguang Ding, Xiao Li, Xiaojun Hu, Yuxi Qiao, Ying Wang, Wujun Xue,

https://doi.org/10.18632/aging.104085 pp 24023—24032

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Li Y, Ding X, Tian X, Zheng J, Ding C, Li X, Hu X, Qiao Y, Wang Y, Xue W, . Islet transplantation modulates macrophage to induce immune tolerance and angiogenesis of islet tissue in type I diabetes mice model. . 12:24023-24032. https://doi.org/10.18632/aging.104085

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                TY  - JOUR
                AU  - Li, Yang 
                AU  - Ding, Xiaoming 
                AU  - Tian, Xiaohui 
                AU  - Zheng, Jin 
                AU  - Ding, Chenguang 
                AU  - Li, Xiao 
                AU  - Hu, Xiaojun 
                AU  - Qiao, Yuxi 
                AU  - Wang, Ying 
                AU  - Xue, Wujun 
                TI  - Islet transplantation modulates macrophage to induce immune tolerance and angiogenesis of islet tissue in type I diabetes mice model
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104085
                DO  - 10.18632/aging.104085
                SP  - 24023
                EP  - 24032
                PY  - 
                AB  - Objective To investigate the dual mechanism of islet transplantation in T1D by regulating the immune tolerance of macrophages and inducing the neovascularization.
                Methods NC group, T1D model group and T1D model + islet group were constructed. Then, the abdominal aorta blood of abdominal aorta and islet tissue were collected. ELISA was performed to detect the level of IL-1R&#x3B1;, IL-1&#x3B1;, IL-1&#x3B2;, CXCL2, MCP1, TNF-&#x3B1; and IL-10. Flow cytometry was used to measure the content of M1 and M2 macrophages. HE staining indicated the pathological characteristics of islet. IHC and WB were applied to determine the protein levels of IGF1R, FGFR2 or VEGFA as well as IGF1R, GRB2, EGFR, PTPN1, JAK2, STAT3, Caspase-1, Bcl2 respectively.
                Results Islet transplantation in T1D stimulated the expression of IL-1R&#x3B1;, IL-1&#x3B1;, IL-1&#x3B2;, CXCL2, MCP1, TNF-&#x3B1; and IL-10 in abdominal aorta blood, changed the content of MHCII+CD206-M1 and MHCII+CD206+M2 macrophages, reduced the pathological features and the infiltration of immunocytes, promoted the expression of IGF1R, FGFR2 and VEGFA, eliminated cell apoptosis and induced the neovascularization in islet grafts.
                Conclusions Islet transplantation is an effective strategy for the treatment of T1D. It can increase the content of M2 macrophages whose immune tolerance can elevate the survival of islet grafts, reduce the inflammatory responses mediated by macrophages, promote the neovascularization and eliminate the cell apoptosis of islet grafts.
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lncRNA DLEU2 acts as a miR-181a sponge to regulate SEPP1 and inhibit skeletal muscle differentiation and regeneration

Yao Wang, Zhi-Jie Zhao, Xue-Ran Kang, Tao Bian, Zhe-Min Shen, Yang Jiang, Bao Sun, Han-Bing Hu, Yi-Sheng Chen,

https://doi.org/10.18632/aging.104095 pp 24033—24056

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Wang Y, Zhao Z, Kang X, Bian T, Shen Z, Jiang Y, Sun B, Hu H, Chen Y, . lncRNA DLEU2 acts as a miR-181a sponge to regulate SEPP1 and inhibit skeletal muscle differentiation and regeneration. . 12:24033-24056. https://doi.org/10.18632/aging.104095

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                TY  - JOUR
                AU  - Wang, Yao 
                AU  - Zhao, Zhi-Jie 
                AU  - Kang, Xue-Ran 
                AU  - Bian, Tao 
                AU  - Shen, Zhe-Min 
                AU  - Jiang, Yang 
                AU  - Sun, Bao 
                AU  - Hu, Han-Bing 
                AU  - Chen, Yi-Sheng 
                TI  - lncRNA DLEU2 acts as a miR-181a sponge to regulate SEPP1 and inhibit skeletal muscle differentiation and regeneration
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104095
                DO  - 10.18632/aging.104095
                SP  - 24033
                EP  - 24056
                PY  - 
                AB  - Sarcopenia is a serious public health problem associated with the loss of muscle mass and function. The purpose of this study was to identify molecular markers and construct a ceRNA pathway as a significant predictor of sarcopenia. We designed a prediction model to select important differentially expressed mRNAs (DEMs), and constructed a sarcopenia associated ceRNA network. After correlation analysis of each element in the ceRNA network based on clinical samples and GTEX database, C2C12 mouse myoblasts were used as a model to verify the identified ceRNA pathways. A new model for predicting sarcopenia based on four molecular markers SEPP1, SV2A, GOT1, and GFOD1 was developed. The model was used to construct a ceRNA network and showed high accuracy. Correlation analysis showed that the expression levels of lncDLEU2, SEPP1, and miR-181a were closely associated with a high risk of sarcopenia. lncDLEU2 inhibits muscle differentiation and regeneration by acting as a miR-181a sponge regulating SEPP1 expression. In this study, a highly accurate prediction tool was developed to improve the prediction outcomes of sarcopenia. These findings suggest that the lncDLEU2-miR-181a-SEPP1 pathway inhibits muscle differentiation and regeneration. This pathway may be a new therapeutic target for the treatment of sarcopenia.
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Age-related DNA methylation changes are sex-specific: a comprehensive assessment

Igor Yusipov, Maria Giulia Bacalini, Alena Kalyakulina, Mikhail Krivonosov, Chiara Pirazzini, Noémie Gensous, Francesco Ravaioli, Maddalena Milazzo, Cristina Giuliani, Maria Vedunova, Giovanni Fiorito, Amedeo Gagliardi, Silvia Polidoro, Paolo Garagnani, Mikhail Ivanchenko, Claudio Franceschi,

https://doi.org/10.18632/aging.202251 pp 24057—24080

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Yusipov I, Bacalini MG, Kalyakulina A, Krivonosov M, Pirazzini C, Gensous N, Ravaioli F, Milazzo M, Giuliani C, Vedunova M, Fiorito G, Gagliardi A, Polidoro S, et al, . Age-related DNA methylation changes are sex-specific: a comprehensive assessment. . 12:24057-24080. https://doi.org/10.18632/aging.202251

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                TY  - JOUR
                AU  - Yusipov, Igor 
                AU  - Bacalini, Maria Giulia 
                AU  - Kalyakulina, Alena 
                AU  - Krivonosov, Mikhail 
                AU  - Pirazzini, Chiara 
                AU  - Gensous, Noémie 
                AU  - Ravaioli, Francesco 
                AU  - Milazzo, Maddalena 
                AU  - Giuliani, Cristina 
                AU  - Vedunova, Maria 
                AU  - Fiorito, Giovanni 
                AU  - Gagliardi, Amedeo 
                AU  - Polidoro, Silvia 
                AU  - Garagnani, Paolo 
                AU  - Ivanchenko, Mikhail 
                AU  - Franceschi, Claudio 
                TI  - Age-related DNA methylation changes are sex-specific: a comprehensive assessment
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202251
                DO  - 10.18632/aging.202251
                SP  - 24057
                EP  - 24080
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Yusipov, Igor 
                AU  - Bacalini, Maria Giulia 
                AU  - Kalyakulina, Alena 
                AU  - Krivonosov, Mikhail 
                AU  - Pirazzini, Chiara 
                AU  - Gensous, Noémie 
                AU  - Ravaioli, Francesco 
                AU  - Milazzo, Maddalena 
                AU  - Giuliani, Cristina 
                AU  - Vedunova, Maria 
                AU  - Fiorito, Giovanni 
                AU  - Gagliardi, Amedeo 
                AU  - Polidoro, Silvia 
                AU  - Garagnani, Paolo 
                AU  - Ivanchenko, Mikhail 
                AU  - Franceschi, Claudio 
                TI  - Age-related DNA methylation changes are sex-specific: a comprehensive assessment
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202251
                DO  - 10.18632/aging.202251
                SP  - 24057
                EP  - 24080
                PY  - 
                AB  - The existence of a sex gap in human health and longevity has been widely documented. Autosomal DNA methylation differences between males and females have been reported, but so far few studies have investigated if DNA methylation is differently affected by aging in males and females. We performed a meta-analysis of 4 large whole blood datasets, comparing 4 aspects of epigenetic age-dependent remodeling between the two sexes: differential methylation, variability, epimutations and entropy. We reported that a large fraction (43%) of sex-associated probes undergoes age-associated DNA methylation changes, and that a limited number of probes show age-by-sex interaction. We experimentally validated 2 regions mapping in FIGN and PRR4 genes and showed sex-specific deviations of their methylation patterns in models of decelerated (centenarians) and accelerated (Down syndrome) aging. While we did not find sex differences in the age-associated increase in epimutations and entropy, we showed that the number of probes having an age-related increase in methylation variability is 15 times higher in males compared to females. Our results can offer new epigenetic tools to study the interaction between aging and sex and can pave the way to the identification of molecular triggers of sex differences in longevity and age-related diseases prevalence.
                ER  -

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Minimizing sedentary behavior (without increasing medium-to-vigorous exercise) associated functional improvement in older women is somewhat dependent on a measurable increase in muscle size

Dale Grant, David Tomlinson, Kostas Tsintzas, Petra Kolić, Gladys Onambélé-Pearson,

https://doi.org/10.18632/aging.202265 pp 24081—24100

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Grant D, Tomlinson D, Tsintzas K, Kolić P, Onambélé-Pearson G, . Minimizing sedentary behavior (without increasing medium-to-vigorous exercise) associated functional improvement in older women is somewhat dependent on a measurable increase in muscle size. . 12:24081-24100. https://doi.org/10.18632/aging.202265

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                TY  - JOUR
                AU  - Grant, Dale 
                AU  - Tomlinson, David 
                AU  - Tsintzas, Kostas 
                AU  - Kolić, Petra 
                AU  - Onambélé-Pearson, Gladys 
                TI  - Minimizing sedentary behavior (without increasing medium-to-vigorous exercise) associated functional
                improvement in older women is somewhat dependent on a measurable increase in muscle size
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202265
                DO  - 10.18632/aging.202265
                SP  - 24081
                EP  - 24100
                PY  - 
                AB  - The optimal pattern of sedentarism displacement and mechanisms underlying its health effects are poorly understood. Therefore, the aim of this study was to quantify muscle-tendon adaptation in response to two different sedentarism displacement interventions and relate any adaptations to functional outcomes. Thirty-four older women (73&#xB1;5yrs) underwent skeletal muscle-tendon size and functional assessments. Participants were randomly allocated to: Sedentary behavior fragmentation (SBF), Light intensity physical activity (LIPA), or Control groups. Measures were taken at weeks 0 and 8. Gait speed significantly increased (p=0.003), in both experimental groups (SBF: 0.06 &#xB1; 0.08m/s, 6&#xB1;10%, LIPA: 0.06 &#xB1; 0.07m/s, 6&#xB1;6%), but not control (-0.02 &#xB1; 0.12m/s, -2&#xB1;9%). Accordingly, the relative change in Vastus Lateralis muscle volume, accounted for 30% (p=0.027), and 45% (p=0.0006) of the explained variance in the relative change in gait speed, for SBF and LIPA respectively. Gastrocnemius Medialis fascicle length changes were positively associated with gait speed changes, following LIPA exclusively (R2= 0.50, p=0.009). This is the first study to show SBF and LIPA are adequate loading in older women, with related muscle adaptation and clinically relevant gait speed improvements. Such adaptations appear similar irrespective of whether sedentarism displacement is prescribed in a single bout (LIPA) or in frequent micro-bouts (SBF).
                ER  -

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Predicting the outcome of non-pharmacological treatment for patients with dementia-related mild cognitive impairment

Yoshihito Shigihara, Hideyuki Hoshi, Jesús Poza, Víctor Rodríguez-González, Carlos Gómez, Takao Kanzawa,

https://doi.org/10.18632/aging.202270 pp 24101—24116

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Shigihara Y, Hoshi H, Poza J, Rodríguez-González V, Gómez C, Kanzawa T, . Predicting the outcome of non-pharmacological treatment for patients with dementia-related mild cognitive impairment. . 12:24101-24116. https://doi.org/10.18632/aging.202270

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                TY  - JOUR
                AU  - Shigihara, Yoshihito 
                AU  - Hoshi, Hideyuki 
                AU  - Poza, Jesús 
                AU  - Rodríguez-González, Víctor 
                AU  - Gómez, Carlos 
                AU  - Kanzawa, Takao 
                TI  - Predicting the outcome of non-pharmacological treatment for patients with dementia-related mild cognitive impairment
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202270
                DO  - 10.18632/aging.202270
                SP  - 24101
                EP  - 24116
                PY  - 
                AB  - Dementia is a progressive cognitive syndrome, with few effective pharmacological treatments that can slow its progress. Hence, non-pharmacological treatments (NPTs) play an important role in improving patient symptoms and quality of life. Designing the optimal personalised NPT strategy relies on objectively and quantitatively predicting the treatment outcome. Magnetoencephalography (MEG) findings can reflect the cognitive status of patients with dementia, and thus potentially predict NPT outcome. In the present study, 16 participants with cognitive impairment underwent NPT for several months. Their cognitive performance was evaluated based on the Mini-Mental State Examination and the Alzheimer&apos;s Disease Assessment Scale - Cognitive at the beginning and end of the NPT period, while resting-state brain activity was evaluated using MEG during the NPT period. Our results showed that the spectral properties of MEG signals predicted the changes in cognitive performance scores. High frequency oscillatory intensity at the right superior frontal gyrus medial segment, opercular part of the inferior frontal gyrus, triangular part of the inferior frontal gyrus, post central gyrus, and angular gyrus predicted the changes in cognitive performance scores. Thus, resting-state brain activity may be a powerful tool in designing personalised NPT.
                ER  -

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Dilated cardiomyopathy impairs mitochondrial biogenesis and promotes inflammation in an age- and sex-dependent manner

Maria Luisa Barcena, Sofya Pozdniakova, Natalie Haritonow, Pavelas Breiter, Anja A. Kühl, Hendrik Milting, Istvan Baczko, Yury Ladilov, Vera Regitz-Zagrosek,

https://doi.org/10.18632/aging.202283 pp 24117—24133

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Barcena ML, Pozdniakova S, Haritonow N, Breiter P, Kühl AA, Milting H, Baczko I, Ladilov Y, Regitz-Zagrosek V, . Dilated cardiomyopathy impairs mitochondrial biogenesis and promotes inflammation in an age- and sex-dependent manner. . 12:24117-24133. https://doi.org/10.18632/aging.202283

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                TY  - JOUR
                AU  - Barcena, Maria Luisa 
                AU  - Pozdniakova, Sofya 
                AU  - Haritonow, Natalie 
                AU  - Breiter, Pavelas 
                AU  - Kühl, Anja A. 
                AU  - Milting, Hendrik 
                AU  - Baczko, Istvan 
                AU  - Ladilov, Yury 
                AU  - Regitz-Zagrosek, Vera 
                TI  - Dilated cardiomyopathy impairs mitochondrial biogenesis and promotes inflammation in an age- and sex-dependent manner
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202283
                DO  - 10.18632/aging.202283
                SP  - 24117
                EP  - 24133
                PY  - 
                AB  - Dilated cardiomyopathy (DCM) belongs to the myocardial diseases associated with a severe impairment of cardiac function, but the question of how sex and age affect this pathology has not been fully explored. Impaired energy homeostasis, mitochondrial dysfunction, and systemic inflammation are well-described phenomena associated with aging. In this study, we investigated if DCM affects these phenomena in a sex- and age-related manner.
                We analyzed the expression of mitochondrial and antioxidant proteins and the inflammatory state in DCM heart tissue from younger and older women and men.
                A significant downregulation of Sirt1 expression was detected in older DCM patients. Sex-related differences were observed in the phosphorylation of AMPK that only appeared in older males with DCM, possibly due to an alternative Sirt1 regulation mechanism. Furthermore, reduced expression of several mitochondrial proteins (TOM40, TIM23, Sirt3, and SOD2) and genes (cox1, nd4) was only detected in old DCM patients, suggesting that age has a greater effect than DCM on these alterations. Finally, an increased expression of inflammatory markers in older, failing hearts, with a stronger pro-inflammatory response in men, was observed. Together, these findings indicate that age- and sex-related increased inflammation and disturbance of mitochondrial homeostasis occurs in male individuals with DCM.
                ER  -

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Detection of NUCB2/nesfatin-1 in cerebrospinal fluid of multiple sclerosis patients

Masaru Shimizu, Taizo Manome, Masumi Kumami, Kouzou Matsumura, Kazuaki Kanai, Kenju Shimomura, Yuko Maejima,

https://doi.org/10.18632/aging.202287 pp 24134—24140

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Shimizu M, Manome T, Kumami M, Matsumura K, Kanai K, Shimomura K, Maejima Y, . Detection of NUCB2/nesfatin-1 in cerebrospinal fluid of multiple sclerosis patients. . 12:24134-24140. https://doi.org/10.18632/aging.202287

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                TY  - JOUR
                AU  - Shimizu, Masaru 
                AU  - Manome, Taizo 
                AU  - Kumami, Masumi 
                AU  - Matsumura, Kouzou 
                AU  - Kanai, Kazuaki 
                AU  - Shimomura, Kenju 
                AU  - Maejima, Yuko 
                TI  - Detection of NUCB2/nesfatin-1 in cerebrospinal fluid of multiple sclerosis patients
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202287
                DO  - 10.18632/aging.202287
                SP  - 24134
                EP  - 24140
                PY  - 
                AB  - NUCB2/nesfatin-1 was originally discovered as an anorexigenic peptide. However, recent studies revealed various additional functions including the regulation of inflammation. However, there are no studies that investigated the involvement of NUCB2/nesfatin-1 in neuroinflammatory diseases. Here, we aimed to investigate the involvement of NUCB2/nesfatin-1 in a representative neuroinflammatory disease, multiple sclerosis (MS).
                Cerebrospinal fluids (CSF) were collected from 24 MS patients and 10 control subjects and NUCB2/nesfatin-1, proinflammatory cytokines (TNF-&#x3B1;, IL-1&#x3B2;) and anti-inflammatory cytokines (IL-10, TGF-&#x3B2;) levels were measured by using ELISA assay. Also the expression of NUCB2/nesfatin-1 in the CSF of MS patient was investigated by western blot analysis.
                Expression of NUCB2/nesfatin-1 was confirmed in the CSF of the MS patient by western blot analysis. NUCB2/nesfatin-1 levels were significantly higher in the CSF of the MS patients. Among the measured cytokines, only IL-1&#x3B2; was lower in the CSF of the MS patients.
                We report for the first time increased NUCB2/nesfatin-1 levels in the CSF of MS patients.
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Accelerated epigenetic age as a biomarker of cardiovascular sensitivity to traffic-related air pollution

Cavin K. Ward-Caviness, Armistead G. Russell, Anne M. Weaver, Erik Slawsky, Radhika Dhingra, Lydia Coulter Kwee, Rong Jiang, Lucas M. Neas, David Diaz-Sanchez, Robert B. Devlin, Wayne E. Cascio, Kenneth Olden, Elizabeth R. Hauser, Svati H. Shah, William E. Kraus,

https://doi.org/10.18632/aging.202341 pp 24141—24155

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Ward-Caviness CK, Russell AG, Weaver AM, Slawsky E, Dhingra R, Kwee LC, Jiang R, Neas LM, Diaz-Sanchez D, Devlin RB, Cascio WE, Olden K, Hauser ER, et al, . Accelerated epigenetic age as a biomarker of cardiovascular sensitivity to traffic-related air pollution. . 12:24141-24155. https://doi.org/10.18632/aging.202341

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                TY  - JOUR
                AU  - Ward-Caviness, Cavin K. 
                AU  - Russell, Armistead G. 
                AU  - Weaver, Anne M. 
                AU  - Slawsky, Erik 
                AU  - Dhingra, Radhika 
                AU  - Kwee, Lydia Coulter 
                AU  - Jiang, Rong 
                AU  - Neas, Lucas M. 
                AU  - Diaz-Sanchez, David 
                AU  - Devlin, Robert B. 
                AU  - Cascio, Wayne E. 
                AU  - Olden, Kenneth 
                AU  - Hauser, Elizabeth R. 
                AU  - Shah, Svati H. 
                AU  - Kraus, William E. 
                TI  - Accelerated epigenetic age as a biomarker of cardiovascular sensitivity to traffic-related air pollution
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202341
                DO  - 10.18632/aging.202341
                SP  - 24141
                EP  - 24155
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Ward-Caviness, Cavin K. 
                AU  - Russell, Armistead G. 
                AU  - Weaver, Anne M. 
                AU  - Slawsky, Erik 
                AU  - Dhingra, Radhika 
                AU  - Kwee, Lydia Coulter 
                AU  - Jiang, Rong 
                AU  - Neas, Lucas M. 
                AU  - Diaz-Sanchez, David 
                AU  - Devlin, Robert B. 
                AU  - Cascio, Wayne E. 
                AU  - Olden, Kenneth 
                AU  - Hauser, Elizabeth R. 
                AU  - Shah, Svati H. 
                AU  - Kraus, William E. 
                TI  - Accelerated epigenetic age as a biomarker of cardiovascular sensitivity to traffic-related air pollution
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202341
                DO  - 10.18632/aging.202341
                SP  - 24141
                EP  - 24155
                PY  - 
                AB  - Background: Accelerated epigenetic age has been proposed as a biomarker of increased aging, which may indicate disruptions in cellular and organ system homeostasis and thus contribute to sensitivity to environmental exposures.
                Methods: Using 497 participants from the CATHGEN cohort, we evaluated whether accelerated epigenetic aging increases cardiovascular sensitivity to traffic-related air pollution (TRAP) exposure. We used residential proximity to major roadways and source apportioned air pollution models as measures of TRAP exposure, and chose peripheral arterial disease (PAD) and blood pressure as outcomes based on previous associations with TRAP. We used Horvath epigenetic age acceleration (AAD) and phenotypic age acceleration (PhenoAAD) as measures of age acceleration, and adjusted all models for chronological age, race, sex, smoking, and socioeconomic status.
                Results: We observed significant interactions between TRAP and both AAD and PhenoAAD. Interactions indicated that increased epigenetic age acceleration elevated associations between proximity to roadways and PAD. Interactions were also observed between AAD and gasoline and diesel source apportioned PM2.5.
                Conclusion: Epigenetic age acceleration may be a biomarker of sensitivity to air pollution, particularly for TRAP in urban cohorts. This presents a novel means by which to understand sensitivity to air pollution and provides a molecular measure of environmental sensitivity.
                ER  -

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Gut microbiota transplantation from db/db mice induces diabetes-like phenotypes and alterations in Hippo signaling in pseudo germ-free mice

Fan Yu, Riyue Jiang, Wei Han, Gaofeng Zhan, Xiaolin Xu, Xiaohong Jiang, Long Wang, Shoukui Xiang, Qin Zhou, Cunming Liu, Bin Zhu, Fei Hua, Chun Yang,

https://doi.org/10.18632/aging.104101 pp 24156—24167

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Yu F, Jiang R, Han W, Zhan G, Xu X, Jiang X, Wang L, Xiang S, Zhou Q, Liu C, Zhu B, Hua F, Yang C, . Gut microbiota transplantation from db/db mice induces diabetes-like phenotypes and alterations in Hippo signaling in pseudo germ-free mice. . 12:24156-24167. https://doi.org/10.18632/aging.104101

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                TY  - JOUR
                AU  - Yu, Fan 
                AU  - Jiang, Riyue 
                AU  - Han, Wei 
                AU  - Zhan, Gaofeng 
                AU  - Xu, Xiaolin 
                AU  - Jiang, Xiaohong 
                AU  - Wang, Long 
                AU  - Xiang, Shoukui 
                AU  - Zhou, Qin 
                AU  - Liu, Cunming 
                AU  - Zhu, Bin 
                AU  - Hua, Fei 
                AU  - Yang, Chun 
                TI  - Gut microbiota transplantation from db/db mice induces diabetes-like phenotypes and alterations in Hippo signaling in pseudo germ-free mice
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104101
                DO  - 10.18632/aging.104101
                SP  - 24156
                EP  - 24167
                PY  - 
                AB  - Type 2 diabetes mellitus (T2DM) is an age-related metabolic disease that is of increasing concern. Gut microbiota might have a critical role in the pathogenesis of T2DM. Additionally, Hippo signaling has been associated strongly with the progression of T2DM and the aging process. We adopted db/db male mice as a T2DM model, and the gut microbiota of db/db and m/m mice were transplanted successfully into pseudo germ-free mice. Furthermore, Hippo signaling, including mammalian sterile 20-like protein kinases 1 (MST1), large tumor suppressors 1 (LATS1), Yes-associated protein (YAP), and phosphorylation of YAP (p-YAP) in peripheral tissues were significantly altered and highly correlated with blood glucose in db/db mice. Interestingly, the host after gut microbiota transplantation from db/db mice showed decreased MST1 and LATS1 levels, and p-YAP/YAP ratio in the heart, liver, and kidney compared to those from m/m mice. Negative correlations between fasting blood glucose and Hippo signaling levels in selected peripheral tissues also were identified. These findings suggest that alterations in Hippo signaling in selected peripheral tissues may contribute to the development of T2DM, and that therapeutic interventions improving Hippo signaling by gut microbiota transplantation might be beneficial for the treatment of T2DM and other age-related metabolic diseases.
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Oxidative stress mediates age-related hypertrophy of ligamentum flavum by inducing inflammation, fibrosis, and apoptosis through activating Akt and MAPK pathways

Hao-Chun Chuang, Kun-Ling Tsai, Kuen-Jer Tsai, Ting-Yuan Tu, Yan-Jye Shyong, I-Ming Jou, Che-Chia Hsu, Shu-Shien Shih, Yuan-Fu Liu, Cheng-Li Lin,

https://doi.org/10.18632/aging.104105 pp 24168—24183

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Chuang H, Tsai K, Tsai K, Tu T, Shyong Y, Jou I, Hsu C, Shih S, Liu Y, Lin C, . Oxidative stress mediates age-related hypertrophy of ligamentum flavum by inducing inflammation, fibrosis, and apoptosis through activating Akt and MAPK pathways. . 12:24168-24183. https://doi.org/10.18632/aging.104105

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                TY  - JOUR
                AU  - Chuang, Hao-Chun 
                AU  - Tsai, Kun-Ling 
                AU  - Tsai, Kuen-Jer 
                AU  - Tu, Ting-Yuan 
                AU  - Shyong, Yan-Jye 
                AU  - Jou, I-Ming 
                AU  - Hsu, Che-Chia 
                AU  - Shih, Shu-Shien 
                AU  - Liu, Yuan-Fu 
                AU  - Lin, Cheng-Li 
                TI  - Oxidative stress mediates age-related hypertrophy of ligamentum flavum by inducing inflammation, fibrosis, and apoptosis through activating Akt and MAPK pathways
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104105
                DO  - 10.18632/aging.104105
                SP  - 24168
                EP  - 24183
                PY  - 
                AB  - The role of oxidative stress in ligamentum flavum (LF) hypertrophy has not been elucidated. We hypothesize that oxidative stress induces inflammatory responses and the subsequent fibrotic processes in LF, via activation of the Akt and MAPK pathways. Specimens of LFs were collected during surgeries for lumbar disc herniation (LDH) or lumbar spinal stenosis (LSS). Part of the LF specimens underwent analyses for ROS, fibrotic markers, and inflammatory mediators, with the remainder minced for cell cultures. The cell cultures were treated with H2O2, after which the cells were lysed and analyzed via western blotting. The specimens of the LSS patients showed increased infiltration of inflammatory cells and were stained positively for MMP-3, MMP-9, vimentin, and fibronectin. The LF of the LSS patients had increased oxidative stress and inflammation compared to that of the LDH patients. In vitro analyses demonstrated that oxidative stress rapidly activated the Akt and MAPK pathways. Inflammatory mediators, iNOS and NF-&#x3BA;B, and fibrotic markers, including TGF-&#x3B2;, &#x3B2;-catenin, &#x3B1;-SMA and vimentin, were significantly upregulated after induction of oxidative stress. Oxidative stress activated the intrinsic apoptotic pathway. These findings revealed that oxidative stress is one of the etiological factors of LF hypertrophy, which might provide new insights into treatment approaches.
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Construction of circRNA-based ceRNA network to reveal the role of circRNAs in the progression and prognosis of metastatic clear cell renal cell carcinoma

Xiyi Wei, Yuxiang Dong, Xinglin Chen, Xiaohan Ren, Guangyao Li, Yamin Wang, Yichun Wang, Tongtong Zhang, Shangqian Wang, Chao Qin, Ninghong Song,

https://doi.org/10.18632/aging.104107 pp 24184—24207

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Wei X, Dong Y, Chen X, Ren X, Li G, Wang Y, Wang Y, Zhang T, Wang S, Qin C, Song N, . Construction of circRNA-based ceRNA network to reveal the role of circRNAs in the progression and prognosis of metastatic clear cell renal cell carcinoma. . 12:24184-24207. https://doi.org/10.18632/aging.104107

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                TY  - JOUR
                AU  - Wei, Xiyi 
                AU  - Dong, Yuxiang 
                AU  - Chen, Xinglin 
                AU  - Ren, Xiaohan 
                AU  - Li, Guangyao 
                AU  - Wang, Yamin 
                AU  - Wang, Yichun 
                AU  - Zhang, Tongtong 
                AU  - Wang, Shangqian 
                AU  - Qin, Chao 
                AU  - Song, Ninghong 
                TI  - Construction of circRNA-based ceRNA network to reveal the role of circRNAs in the progression and prognosis of metastatic clear cell renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104107
                DO  - 10.18632/aging.104107
                SP  - 24184
                EP  - 24207
                PY  - 
                AB  - CircRNAs are now under hot discussion as novel promising bio-markers for patients with clear cell renal cell carcinoma. The purpose of our study is to identify several circRNAs related to the metastasis and progression of clear cell renal cell carcinoma, and to further investigate the mechanism of their influence on tumor progression. The transcriptome data of ccRCC and clinical characteristics used in this study were downloaded from the The Cancer Genome Atlas and Gene Expression Omnibus database. A total of 114 circRNAs were found to be related to tumor initiation, progression and metastasis after the intersection. In addition, 14 miRNAs and 201 eligible mRNAs were selected as targets gene, respectively. CeRNA network was constructed based on 8 circRNAs, 14 miRNAs, and 201 mRNAs. Besides, another 6 hub genes were identified via the PPI network. It should be noted that only TRIM2 was confirmed as an independent prognostic factor, which was simultaneously significantly related to both clinical stage and pathological grade in clinical cohorts. Kyoto Encyclopedia of Genes and Genomes and Gene Ontology analysis indicated the possible function of TRIM2 in ccRCC progression, such as ubiquitin mediated protein hydrolysis, cell adhesion molecules, Th17 cell differentiation signaling pathway and so on. Gene set enrichment analysis analysis revealed that TRIM2 may be involved in ubiquitin mediated proteolysis, apoptosis, autophagy and citrate cycle TCA cycle. Hub circ_RNAs expressions were validated in ccRCC tissues and cell lines. Our study revealed that the hsa_circ_0002286 / has-mir-222-5p / TRIM2 axis played a critical role in the progression of ccRCC. Specifically, it may inhibit the metastasis and progression of ccRCC, which could serve as a potential therapeutic target.
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SRT2183 impairs ovarian cancer by facilitating autophagy

Tingting Sun, Yanfen Hu, Weipeng He, Yuru Shang, Xiaohong Yang, Liyun Gong, Xianbin Zhang, Peng Gong, Guofen Yang,

https://doi.org/10.18632/aging.104126 pp 24208—24218

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Sun T, Hu Y, He W, Shang Y, Yang X, Gong L, Zhang X, Gong P, Yang G, . SRT2183 impairs ovarian cancer by facilitating autophagy. . 12:24208-24218. https://doi.org/10.18632/aging.104126

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                TY  - JOUR
                AU  - Sun, Tingting 
                AU  - Hu, Yanfen 
                AU  - He, Weipeng 
                AU  - Shang, Yuru 
                AU  - Yang, Xiaohong 
                AU  - Gong, Liyun 
                AU  - Zhang, Xianbin 
                AU  - Gong, Peng 
                AU  - Yang, Guofen 
                TI  - SRT2183 impairs ovarian cancer by facilitating autophagy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104126
                DO  - 10.18632/aging.104126
                SP  - 24208
                EP  - 24218
                PY  - 
                AB  - The 5-year survival rate of ovarian cancer patients is only 47%, and developing novel drugs for ovarian cancer is needed. Herein, we evaluated if and how SRT2183, a sirtuin-1 activator, impairs the ovarian cancer cells. OVCAR-3 and A2780 cells were treated with SRT2183. Cell viability was measured by cell counting kit-8 assay and clonogenic assay. Apoptosis was determined by flow cytometry with Annexin V and propidium iodide. The level of autophagy was evaluated by western blot and immunofluorescence. The activities of AKT/mTOR/70s6k and MAPK signaling pathway were measured by immunoblot. SRT2183 inhibited the growth of ovarian cancer cells, increased the accumulation of BAX, cleaved-caspase 3 and cleaved-PARP, and decreased the level of anti-apoptotic Bcl-2 and Mcl-1. SRT2183 increased the LC3II level, and enhanced the degradation of p62/SQSTM1. SRT2183 increased the formation of GFP-LC3 puncta and induced the maturation of autophagosome. Interestingly, knockdown of autophagy related 5 and 7 significantly impaired the anti-carcinoma activity of SRT2183, implying that SRT2183 impaired the ovarian cancer cells by inducing autophagy. SRT2183 decreased the accumulation of p-Akt, p-mTOR and p-70s6k, and activated the p38 MAPK signaling pathway. This indicated that Akt/mTOR/70s6k and p38 MAPK signaling pathway might be involved in the SRT2183-mediated autophagy and apoptosis.
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Stroke risk in hypertrophic cardiomyopathy patients with atrial fibrillation: a nationwide database study

Jung-Chi Hsu, Ya-Ting Huang, Lian-Yu Lin,

https://doi.org/10.18632/aging.104133 pp 24219—24227

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Hsu J, Huang Y, Lin L, . Stroke risk in hypertrophic cardiomyopathy patients with atrial fibrillation: a nationwide database study. . 12:24219-24227. https://doi.org/10.18632/aging.104133

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                TY  - JOUR
                AU  - Hsu, Jung-Chi 
                AU  - Huang, Ya-Ting 
                AU  - Lin, Lian-Yu 
                TI  - Stroke risk in hypertrophic cardiomyopathy patients with atrial fibrillation: a nationwide database study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104133
                DO  - 10.18632/aging.104133
                SP  - 24219
                EP  - 24227
                PY  - 
                AB  - Current treatment guidelines recommend anticoagulation for hypertrophic cardiomyopathy (HCM) with atrial fibrillation (AF) regardless of the CHA2DS2-VASc score. As aging and stroke risk factors (hypertension, diabetes mellitus) are confounders of ischemic stroke, young patients with a low stroke risk may not need anticoagulant treatment. This study aimed to determine the incidence of stroke and its risk factors in HCM patients with AF during a long-term follow-up. Using a national database, we retrospectively investigated 18,724 HCM patients from a systematic sample of 1,000,000 Taiwanese people between 1997 and 2013. The incidences of AF and stroke were estimated. Data were analyzed using Cox regression models. AF was identified in 598 patients (262 men, mean age 66.3&#xB1;13.0 years) during a median follow-up of 7.0 years. The AF incidence in HCM patients was 5.83 per 1000 person-years, and the overall incidence of AF-associated stroke was 24.14 per 1000 person-years. The incidence of transient ischemic attack (TIA)/ischemic stroke varied from 20.41 to 60.55 per 1000 person-years, without proportionality to CHA2DS2-VASc score increase. Among patients aged &lt;40 years, none experienced TIA/ischemic stroke. Univariate Cox regression models showed that age (p&lt;0.001), prior TIA/ischemic stroke (p=0.02), and CHA2DS2-VASc score (p=0.003) were risk factors for TIA/ischemic stroke. Multivariate analysis indicated that age (hazard ratio 1.04, 95% confidence interval [CI] 1.02-1.06, p=0.001) and prior TIA/ischemic stroke (hazard ratio 2.82, 95% CI 1.27-6.25, p=0.011) were independently associated with TIA/ischemic stroke. Taiwanese patients with concomitant HCM and AF have a high stroke risk regardless of the CHA2DS2-VASc score. Aging is the main predictor. As the overall incidence of stroke was low in young patients, anticoagulants may not be needed in this subpopulation.
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The value of a metabolic reprogramming-related gene signature for pancreatic adenocarcinoma prognosis prediction

Zhen Tan, Yubin Lei, Jin Xu, Si Shi, Jie Hua, Bo Zhang, Qingcai Meng, Jiang Liu, Yiyin Zhang, Miaoyan Wei, Xianjun Yu, Chen Liang,

https://doi.org/10.18632/aging.104134 pp 24228—24241

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Tan Z, Lei Y, Xu J, Shi S, Hua J, Zhang B, Meng Q, Liu J, Zhang Y, Wei M, Yu X, Liang C, . The value of a metabolic reprogramming-related gene signature for pancreatic adenocarcinoma prognosis prediction. . 12:24228-24241. https://doi.org/10.18632/aging.104134

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                TY  - JOUR
                AU  - Tan, Zhen 
                AU  - Lei, Yubin 
                AU  - Xu, Jin 
                AU  - Shi, Si 
                AU  - Hua, Jie 
                AU  - Zhang, Bo 
                AU  - Meng, Qingcai 
                AU  - Liu, Jiang 
                AU  - Zhang, Yiyin 
                AU  - Wei, Miaoyan 
                AU  - Yu, Xianjun 
                AU  - Liang, Chen 
                TI  - The value of a metabolic reprogramming-related gene signature for pancreatic adenocarcinoma prognosis prediction
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104134
                DO  - 10.18632/aging.104134
                SP  - 24228
                EP  - 24241
                PY  - 
                AB  - Pancreatic ductal adenocarcinoma (PDAC) is one of the most fatal malignancies worldwide. Extensive enhancement of glycolysis and reprogramming of lipid metabolism are both associated with the development and progression of PDAC. Previous studies have suggested that various gene signatures could convey prognostic information about PDAC. However, the use of these signatures has some limitations, perhaps because of a lack of knowledge regarding the genetic and energy supply backgrounds of PDAC. Therefore, we conducted multi-mRNA analysis based on metabolic reprogramming to identify novel signatures for accurate prognosis prediction in PDAC patients. In this study, a three-gene signature comprising MET, ENO3 and CD36 was established to predict the overall survival of PDAC patients. The three-gene signature could divide patients into high- and low-risk groups by disparities in overall survival verified by log-rank test in two independent validation cohorts and could differentiate tumors from normal tissues with excellent accuracy in four Gene Expression Omnibus (GEO) cohorts. We also found a positive correlation between the risk score of the gene signature and inherited germline mutations in PDAC predisposition genes. A glycolysis and lipid metabolism-based gene nomogram and corresponding calibration curves showed significant performance for survival prediction in the TCGA-PDAC dataset. The high-risk designation was closely connected with oncological signatures and multiple aggressiveness-related pathways, as determined by gene set enrichment analysis (GSEA). In summary, our study developed a three-gene signature and established a prognostic nomogram that objectively predicted overall survival in PDAC. The findings could provide a reference for the prediction of overall survival and could aid in individualized management for PDAC patients.
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TNFAIP3 ameliorates the degeneration of inflammatory human nucleus pulposus cells by inhibiting mTOR signaling and promoting autophagy

Jie Chen, Yufei Ma, Zhijie Yang, Haiyang Lan, Guangliang Liu, Ye Zhang, Huiqiang Xia, Xiaofang Wang, Fei Han, Xiaolin Tu, Bo Liu,

https://doi.org/10.18632/aging.104160 pp 24242—24254

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Chen J, Ma Y, Yang Z, Lan H, Liu G, Zhang Y, Xia H, Wang X, Han F, Tu X, Liu B, . TNFAIP3 ameliorates the degeneration of inflammatory human nucleus pulposus cells by inhibiting mTOR signaling and promoting autophagy. . 12:24242-24254. https://doi.org/10.18632/aging.104160

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                TY  - JOUR
                AU  - Chen, Jie 
                AU  - Ma, Yufei 
                AU  - Yang, Zhijie 
                AU  - Lan, Haiyang 
                AU  - Liu, Guangliang 
                AU  - Zhang, Ye 
                AU  - Xia, Huiqiang 
                AU  - Wang, Xiaofang 
                AU  - Han, Fei 
                AU  - Tu, Xiaolin 
                AU  - Liu, Bo 
                TI  - TNFAIP3 ameliorates the degeneration of inflammatory human nucleus pulposus cells by inhibiting mTOR signaling and promoting autophagy
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104160
                DO  - 10.18632/aging.104160
                SP  - 24242
                EP  - 24254
                PY  - 
                AB  - Autophagy is involved in degenerative diseases such as osteoarthritis and disc degeneration. Although, tumor necrosis factor &#x3B1;-induced protein 3 (TNFAIP3) is well-known as a key regulator of inflammation and autophagy, it is still not clear whether TNFAIP3 regulates autophagy to protect from human disc cells degeneration. We hypothesize that TNFAIP3 may also regulate autophagy to inhibit pro-inflammatory cytokines expression in human nucleus pulposus cells (NPCs). In this study, TNFAIP3 expression was increased in degenerative disc tissue as well as LPS-stimulated human NPCs, and the effect of TNFAIP3 in LPS-induced NPCs was further explored. The results demonstrated that pro-inflammatory cytokines expression in TNFAIP3-His cells was decreased, while it was increased in TNFAIP3-siRNA cells. Further molecular mechanism research showed that TNFAIP3-siRNA cells enhanced the phosphorylation of mammalian target of rapamycin (mTOR) and inhibited autophagy. Meanwhile, after treatment of TNFAIP3-siRNA cells with the mTOR inhibitor Torin1, the level of autophagy increased and the decrease of extracellular matrix was reversed. In summary, overexpressed TNFAIP3 can promote autophagy and reduce inflammation in LPS-induced human NPCs. Moreover, autophagy triggered by TNFAIP3 can ameliorate the degeneration of inflammatory human NPCs, providing a potential and an attractive therapeutic strategy for degenerative disease.
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Exploring the mechanism of resistance to sorafenib in two hepatocellular carcinoma cell lines

Zhi Zhang, Cheng-Zu He, Ya-Qin Qin, Jian-Jun Liao, Shang-Tao Huang, Steven Mo, Hong-Mian Li, Jian-Yan Lin,

https://doi.org/10.18632/aging.104195 pp 24255—24269

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Zhang Z, He C, Qin Y, Liao J, Huang S, Mo S, Li H, Lin J, . Exploring the mechanism of resistance to sorafenib in two hepatocellular carcinoma cell lines. . 12:24255-24269. https://doi.org/10.18632/aging.104195

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                TY  - JOUR
                AU  - Zhang, Zhi 
                AU  - He, Cheng-Zu 
                AU  - Qin, Ya-Qin 
                AU  - Liao, Jian-Jun 
                AU  - Huang, Shang-Tao 
                AU  - Mo, Steven 
                AU  - Li, Hong-Mian 
                AU  - Lin, Jian-Yan 
                TI  - Exploring the mechanism of resistance to sorafenib in two hepatocellular carcinoma cell lines
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104195
                DO  - 10.18632/aging.104195
                SP  - 24255
                EP  - 24269
                PY  - 
                AB  - Sorafenib has long been the only approved systemic therapy for advanced hepatocellular carcinoma (HCC), but most patients show primary or acquired drug resistance. In the present study, RNA was extracted from sorafenib-resistant and -sensitive clones of the HCC cell lines HepG2 and Huh7. Protein-protein interaction networks of the up- and down-regulated genes common to the two sorafenib-resistant cell lines were extracted and subjected to modular analysis in order to identify functional modules. Functional enrichment analysis showed the modules were involved in different biological processes and pathways. These results indicate that sorafenib resistance in HCC is complicated and heterogeneous. The potential regulators of each functional module, including transcription factors, microRNAs and long non-coding RNAs, were explored to construct a comprehensive transcriptional regulatory network related to sorafenib resistance in HCC. Our results provide new insights into sorafenib resistance of HCC at the level of transcriptional regulation.
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Metformin protects against myocardial ischemia-reperfusion injury and cell pyroptosis via AMPK/NLRP3 inflammasome pathway

Jing Zhang, Lelin Huang, Xing Shi, Liu Yang, Fuzhou Hua, Jianyong Ma, Wengen Zhu, Xiao Liu, Rui Xuan, Yunfeng Shen, Jianping Liu, Xiaoyang Lai, Peng Yu,

https://doi.org/10.18632/aging.202143 pp 24270—24287

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Zhang J, Huang L, Shi X, Yang L, Hua F, Ma J, Zhu W, Liu X, Xuan R, Shen Y, Liu J, Lai X, Yu P, . Metformin protects against myocardial ischemia-reperfusion injury and cell pyroptosis via AMPK/NLRP3 inflammasome pathway. . 12:24270-24287. https://doi.org/10.18632/aging.202143

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                TY  - JOUR
                AU  - Zhang, Jing 
                AU  - Huang, Lelin 
                AU  - Shi, Xing 
                AU  - Yang, Liu 
                AU  - Hua, Fuzhou 
                AU  - Ma, Jianyong 
                AU  - Zhu, Wengen 
                AU  - Liu, Xiao 
                AU  - Xuan, Rui 
                AU  - Shen, Yunfeng 
                AU  - Liu, Jianping 
                AU  - Lai, Xiaoyang 
                AU  - Yu, Peng 
                TI  - Metformin protects against myocardial ischemia-reperfusion injury and cell pyroptosis via AMPK/NLRP3 inflammasome pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202143
                DO  - 10.18632/aging.202143
                SP  - 24270
                EP  - 24287
                PY  - 
                AB  - Ischemia/reperfusion (I/R) injury is a life-threatening vascular emergency following myocardial infarction. Our previous study showed cardioprotective effects of metformin against myocardial I/R injury. In this study, we further examined the involvement of AMPK mediated activation of NLRP3 inflammasome in this cardioprotective effect of metformin. Myocardial I/R injury was simulated in a rat heart Langendorff model and neonatal rat ventricle myocytes (NRVMs) were subjected to hypoxi/reoxygenation (H/R) to establish an in vitro model. Outcome measures included myocardial infarct size, hemodynamic monitoring, myocardial tissue injury, myocardial apoptotic index and the inflammatory response. myocardial infarct size and cardiac enzyme activities. First, we found that metformin postconditioning can not only significantly alleviated myocardial infarct size, attenuated cell apoptosis, and inhibited myocardial fibrosis. Furthermore, metformin activated phosphorylated AMPK, decreased pro-inflammatory cytokines, TNF-&#x3B1;, IL-6 and IL-1&#x3B2;, and decreased NLRP3 inflammasome activation. In isolated NRVMs metformin increased cellular viability, decreased LDH activity and inhibited cellular apoptosis and inflammation. Importantly, inhibition of AMPK phosphorylation by Compound C (CC) resulted in decreased survival of cardiomyocytes mainly by inducing the release of inflammatory cytokines and increasing NLRP3 inflammasome activation. Finally, in vitro studies revealed that the NLRP3 activator nigericin abolished the anti-inflammatory effects of metformin in NRVMs, but it had little effect on AMPK phosphorylation. Collectively, our study confirmed that metformin exerts cardioprotective effects by regulating myocardial I/R injury-induced inflammatory response, which was largely dependent on the enhancement of the AMPK pathway, thereby suppressing NLRP3 inflammasome activation.
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Sensory impairment and all-cause mortality among the elderly adults in China: a population-based cohort study

Ji Sun, Lin Li, Jiangwei Sun,

https://doi.org/10.18632/aging.202198 pp 24288—24300

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Sun J, Li L, Sun J, . Sensory impairment and all-cause mortality among the elderly adults in China: a population-based cohort study. . 12:24288-24300. https://doi.org/10.18632/aging.202198

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                TY  - JOUR
                AU  - Sun, Ji 
                AU  - Li, Lin 
                AU  - Sun, Jiangwei 
                TI  - Sensory impairment and all-cause mortality among the elderly adults in China: a population-based cohort study
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202198
                DO  - 10.18632/aging.202198
                SP  - 24288
                EP  - 24300
                PY  - 
                AB  - With age-related functional deterioration, sensory impairment including vision impairment (VI), hearing impairment (HI), and dual sensory impairment (DSI) usually occurred among the elderly population, causing a decrease in functional capacity and quality of life. The study aimed to explore how sensory impairment is associated with the risk of all-cause mortality among the elderly adults in China. We prospectively investigated the association among 37,076 participants enrolled from 1998 to 2019 in the Chinese Longitudinal Healthy Longevity Survey. We also, as a sensitivity analysis, explored the association among 11,365 newly incident sensory impairment participants. Cox regression model with sensory impairment as a time-varying exposure was performed to calculate the hazard ratios (HRs) and 95% confidence intervals (CIs). Compared with participants without sensory impairment, those with VI (HR=1.20, 95% CI: 1.15-1.24), HI (HR=1.26, 95% CI: 1.21-1.31), and DSI (HR: 1.46, 95% CI=1.41-1.52) had significant higher risk of all-cause mortality after adjusting for potential confounders. These associations were robust among subgroup analyses stratified by sex and entry age, and sensitivity analyses performed among newly incident sensory impairment participants. In conclusion, sensory impairment was associated with higher mortality risk among the elderly adults in China.
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Cigarette smoke extract induces airway epithelial cell death via repressing PRMT6/AKT signaling

Tiao Li, Kristen V. Fanning, Toru Nyunoya, Yan Chen, Chunbin Zou,

https://doi.org/10.18632/aging.202210 pp 24301—24317

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Li T, Fanning KV, Nyunoya T, Chen Y, Zou C, . Cigarette smoke extract induces airway epithelial cell death via repressing PRMT6/AKT signaling. . 12:24301-24317. https://doi.org/10.18632/aging.202210

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                TY  - JOUR
                AU  - Li, Tiao 
                AU  - Fanning, Kristen V. 
                AU  - Nyunoya, Toru 
                AU  - Chen, Yan 
                AU  - Zou, Chunbin 
                TI  - Cigarette smoke extract induces airway epithelial cell death via repressing PRMT6/AKT signaling
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202210
                DO  - 10.18632/aging.202210
                SP  - 24301
                EP  - 24317
                PY  - 
                AB  - Chronic obstructive pulmonary disease (COPD) is a severe public health threat world-wide. Cigarette smoke (CS)-induced airway epithelial cell death is a major pathway of pathogenesis in emphysema, a subtype of COPD. Protein arginine methyltransferase 6 (PRMT6) is a type I PRMT that catalyzes mono- and di-methylation on arginine residues within histone and non-histone proteins to modulate a variety of life processes, such as apoptosis. However, its role in CS-induced lung epithelial death has not been fully elucidated. Here we report that PRMT6 was decreased in mouse lung tissues from a cigarette smoke extract (CSE)-mediated experimental emphysematous model and in CSE treated or cigarette smoke exposed lung epithelial cells. Depletion of PRMT6 increased the protein levels of phosphatase PTEN and PI3K regulatory subunit p85 but decreased a downstream kinase PDK1, resulting in AKT dephosphorylation and thereafter, lung epithelial cell death. Knockout of PRMT6 inhibited epithelial survival and promoted CSE-mediated epithelial cell death, while ectopic expression of PRMT6 protein partially reversed epithelial cell death via PI3K/AKT-mediated cell survival signaling in CSE cellular models. These findings demonstrate that PRMT6 plays a crucial role in CS-induced bronchial epithelial cell death that may be a potential therapeutic target against the airway cell death in CS-induced COPD.
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Isoquercitrin induces apoptosis and autophagy in hepatocellular carcinoma cells via AMPK/mTOR/p70S6K signaling pathway

Liyan Shui, Weina Wang, Mingjie Xie, Bingjue Ye, Xian Li, Yanning Liu, Min Zheng,

https://doi.org/10.18632/aging.202237 pp 24318—24332

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Shui L, Wang W, Xie M, Ye B, Li X, Liu Y, Zheng M, . Isoquercitrin induces apoptosis and autophagy in hepatocellular carcinoma cells via AMPK/mTOR/p70S6K signaling pathway. . 12:24318-24332. https://doi.org/10.18632/aging.202237

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                TY  - JOUR
                AU  - Shui, Liyan 
                AU  - Wang, Weina 
                AU  - Xie, Mingjie 
                AU  - Ye, Bingjue 
                AU  - Li, Xian 
                AU  - Liu, Yanning 
                AU  - Zheng, Min 
                TI  - Isoquercitrin induces apoptosis and autophagy in hepatocellular carcinoma cells via AMPK/mTOR/p70S6K signaling pathway
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202237
                DO  - 10.18632/aging.202237
                SP  - 24318
                EP  - 24332
                PY  - 
                AB  - Hepatocellular carcinoma (HCC) is an aggressive malignancy with high rates of metastasis and relapse. Isoquercitrin (ISO), a natural flavonoid present in the Chinese bayberry and other plant species, reportedly exerts notable inhibitory effects on tumor cell proliferation, though the mechanism is unknown. In the present study, we exposed HepG2 and Huh7 human liver cancer cells to ISO and examined the roles of autophagy and apoptosis in ISO-mediated cell death. We found that ISO exposure inhibited cell viability and colony growth, activated apoptotic pathway, and triggered dysregulated autophagy by activating the AMPK/mTOR/p70S6K pathway. Autophagy inhibition using 3-methyladenine (3-MA) or Atg5-targeted siRNA decreased the Bax/Bcl-2 ratio, caspase-3 activation, and PARP cleavage and protected cells against ISO-induced apoptosis. Moreover, autophagy inhibition reversed the upregulation of AMPK phosphorylation and downregulation of mTOR and p70S6K phosphorylation elicited by ISO. By contrast, application of a broad-spectrum caspase inhibitor failed to inhibit autophagy in ISO-treated cells. These data indicate that ISO simultaneously induced apoptosis and autophagy, and abnormal induction of autophagic flux contributed to ISO-triggered caspase-3-dependent apoptosis.
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Intra-tumoral heterogeneity and immune responses predicts prognosis of gastric cancer

Wanjing Feng, Yue Wang, Siyuan Chen, Xiaodong Zhu,

https://doi.org/10.18632/aging.202238 pp 24333—24344

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Feng W, Wang Y, Chen S, Zhu X, . Intra-tumoral heterogeneity and immune responses predicts prognosis of gastric cancer. . 12:24333-24344. https://doi.org/10.18632/aging.202238

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                TY  - JOUR
                AU  - Feng, Wanjing 
                AU  - Wang, Yue 
                AU  - Chen, Siyuan 
                AU  - Zhu, Xiaodong 
                TI  - Intra-tumoral heterogeneity and immune responses predicts prognosis of gastric cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202238
                DO  - 10.18632/aging.202238
                SP  - 24333
                EP  - 24344
                PY  - 
                AB  - Chemotherapy resistance eventually develops in patients with gastric cancer (GC). Intra-tumoral heterogeneity (ITH) refers to the intercellular genetic variations and phenotypic diversity that affect responses to drug therapy. We measured ITH using mutant-allele tumor heterogeneity (MATH) derived from whole-exome sequencing data of patients with GC in The Cancer Genome Atlas (TCGA) database. The study included 385 patients from the TCGA database with available data regarding gastrectomy, survival, and whole-exome sequencing. Further analysis was performed in 171 GC patients with available data regarding adjuvant chemotherapy. Multiple factor analysis showed that MATH was an independent predictor of OS (hazard ratio [HR], 1.432; 95% confidence interval [CI], 1.073&#x2013;1.913; P = 0.015) in patients with GC. Moreover, MATH was also an independent predictor of OS among the 171 GC patients who received adjuvant chemotherapy (HR, 2.016; 95% CI, 1.236&#x2013;3.289; P = 0.005). Pathway enrichment and immune cell analyses revealed significantly higher infiltration by 20 types of immune cells in the low/intermediate group, compared to the group with high MATH scores. In conclusion, low/intermediate MATH scores predicted longer OS, when compared to those with high MATH scores. The immune response was obviously upregulated in patients with GC and low/intermediate MATH scores.
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Implication of integrins α3β1 and α5β1 in invasion and anoikis of SK-Mel-147 human melanoma cells: non-canonical functions of protein kinase Akt

Nadezhda I. Kozlova, Galina E. Morozevich, Nina M. Gevorkian, Albert E. Berman,

https://doi.org/10.18632/aging.202243 pp 24345—24356

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Kozlova NI, Morozevich GE, Gevorkian NM, Berman AE, . Implication of integrins α3β1 and α5β1 in invasion and anoikis of SK-Mel-147 human melanoma cells: non-canonical functions of protein kinase Akt. . 12:24345-24356. https://doi.org/10.18632/aging.202243

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                TY  - JOUR
                AU  - Kozlova, Nadezhda I. 
                AU  - Morozevich, Galina E. 
                AU  - Gevorkian, Nina M. 
                AU  - Berman, Albert E. 
                TI  - Implication of integrins α3β1 and α5β1 in invasion and anoikis of SK-Mel-147 human melanoma cells: non-canonical functions of protein kinase Akt
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202243
                DO  - 10.18632/aging.202243
                SP  - 24345
                EP  - 24356
                PY  - 
                AB  - Downregulation of integrins &#x3B1;3&#x3B2;1 and &#x3B1;5&#x3B2;1 strongly decreased cell colony formation and in vitro invasion and markedly enhanced anoikis in SK-Mel-147 human melanoma cells. These modifications were accompanied by a marked increase in the levels of active Akt protein kinase, which indicated it played a non-canonical function in the melanoma cells. Pharmacological inhibition of Akt1, an Akt isozyme, in cells depleted of &#x3B1;3&#x3B2;1 or &#x3B1;5&#x3B2;1 restored their invasive activity, while inhibition of the Akt 2 isoform did not cause a visible effect. Similar to our previous results with the &#x3B1;2&#x3B2;1 integrin, this finding suggested that in signaling pathways initiated by &#x3B1;3&#x3B2;1 and &#x3B1;5&#x3B2;1, the Akt1 isoform performs a non-canonical function in regulating invasive phenotype of melanoma cells. In contrast, when the effects of Akt inhibitors on anoikis of the melanoma cells were compared, the Akt2 isoform demonstrated a non-canonical activity in which Akt2 suppression led to a significant attenuation of apoptosis in cells with downregulated &#x3B1;3&#x3B2;1 or &#x3B1;5&#x3B2;1. Our results were the first evidence that, in the same tumor cells, different integrins can control various manifestations of tumor progression through distinct signaling pathways that are both common to various integrins and specific to a particular receptor.
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A forced swim-based rat model of premenstrual depression: effects of hormonal changes and drug intervention

Sheng Wei, Xiwen Geng, Zifa Li, Kaiyong Xu, Minghui Hu, Hongyun Wu, Wei Shi, Mingqi Qiao,

https://doi.org/10.18632/aging.202249 pp 24357—24370

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Wei S, Geng X, Li Z, Xu K, Hu M, Wu H, Shi W, Qiao M, . A forced swim-based rat model of premenstrual depression: effects of hormonal changes and drug intervention. . 12:24357-24370. https://doi.org/10.18632/aging.202249

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                TY  - JOUR
                AU  - Wei, Sheng 
                AU  - Geng, Xiwen 
                AU  - Li, Zifa 
                AU  - Xu, Kaiyong 
                AU  - Hu, Minghui 
                AU  - Wu, Hongyun 
                AU  - Shi, Wei 
                AU  - Qiao, Mingqi 
                TI  - A forced swim-based rat model of premenstrual depression: effects of hormonal changes and drug intervention
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202249
                DO  - 10.18632/aging.202249
                SP  - 24357
                EP  - 24370
                PY  - 
                AB  - Premenstrual dysphoric disorder (PMDD), a form of premenstrual syndrome (PMS), is a severe health disturbance that affects a patient&#x2019;s emotions; it is caused by periodic psychological symptoms, and its pathogenesis remains unclear. As depression-like symptoms are found in a majority of clinical cases, a reliable animal model of premenstrual depression is indispensable to understand the pathogenesis. Herein, we describe a novel rat model of premenstrual depression, based on the forced swimming test, with a regular estrous cycle. The results showed that in the estrous cycle, the depression-like behavior of rats occurred in the non-receptive phase and disappeared in the receptive phase. Following ovariectomy, the depression-like symptoms disappeared and returned after a hormone priming regimen. Moreover, fluoxetine, an anti-depressant, could reverse the behavioral symptoms in these model rats with normal estrous cycle. Further, the model rats showed significant changes in the serum levels of estrogen and progesterone, hippocampal levels of allopregnanolone, 5-hydroxytryptamine, norepinephrine, and &#x3B3;-aminobutyric acid (GABA), and in the expression of GABAA receptor 4&#x3B1; subunit, all of which were reversed to physiological levels by fluoxetine. Overall, we established a reliable and standardized rat model of premenstrual depression, which may facilitate the elucidation of PMS/PMDD pathogenesis and development of related therapies.
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Mental awareness improved mild cognitive impairment and modulated gut microbiome

Wei Wei Thwe Khine, Miao Lian Voong, Ted Kheng Siang Ng, Lei Feng, Grishma Avinash Rane, Alan Prem Kumar, Ee Heok Kua, Ratha Mahendran, Rathi Mahendran, Yuan-Kun Lee,

https://doi.org/10.18632/aging.202277 pp 24371—24393

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Khine WWT, Voong ML, Ng TKS, Feng L, Rane GA, Kumar AP, Kua EH, Mahendran R, Mahendran R, Lee Y, . Mental awareness improved mild cognitive impairment and modulated gut microbiome. . 12:24371-24393. https://doi.org/10.18632/aging.202277

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                TY  - JOUR
                AU  - Khine, Wei Wei Thwe 
                AU  - Voong, Miao Lian 
                AU  - Ng, Ted Kheng Siang 
                AU  - Feng, Lei 
                AU  - Rane, Grishma Avinash 
                AU  - Kumar, Alan Prem 
                AU  - Kua, Ee Heok 
                AU  - Mahendran, Ratha 
                AU  - Mahendran, Rathi 
                AU  - Lee, Yuan-Kun 
                TI  - Mental awareness improved mild cognitive impairment and modulated gut microbiome
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202277
                DO  - 10.18632/aging.202277
                SP  - 24371
                EP  - 24393
                PY  - 
                AB  - There is ample scientific and clinical evidence of the effects of gut microbiota on the brain but no definitive evidence that the brain can affect changes in gut microbiota under the bi-directional gut-brain axis concept. As there is no pharmacotherapeutic intervention for the early stages of cognitive decline, research has focused on cognitive stimulation in reversing or slowing the impairment. Elderly patients diagnosed with mild cognitive impairment underwent a randomized-control trial of mindful awareness practice. Neuropsychological assessments, inflammatory markers, and gut microbiota profiles were tested. Here, we report that their cognitive impairment was improved and associated with changes in gut bacterial profile. A cognition-score-dependent-abundance was observed in Ruminococcus vs Recognition Trials (RT), Digit Span Backward (DSB), Semantic Fluency Span (SFS) and Memory Domain (MD); Coprococcus vs DSB, Color Trails Test 2 (CTT2) and Block Design (BD); Parabacteroides vs DSB and SFS; Fusobacterium vs DSB and CTT2; Enterobacteriaceae vs BD and SFS; Ruminococcaceae vs DSB; Phascolarctobacterium vs MD. The study showed for the first-time, alteration in the cognitive capacity leading to the corresponding changes in microbiota profiles. This strongly suggests that signals from the different segments of brain could dictate directly or indirectly the abundances of specific gut microbes.
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E3 ligase FBXW7 restricts M2-like tumor-associated macrophage polarization by targeting c-Myc

Lijia Zhong, Yuanyuan Zhang, Mengyao Li, Yinjing Song, Danhui Liu, Xin Yang, Dehua Yang, Hao Qu, Lihua Lai, Qingqing Wang, Zhimin Chen,

https://doi.org/10.18632/aging.202293 pp 24394—24423

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Zhong L, Zhang Y, Li M, Song Y, Liu D, Yang X, Yang D, Qu H, Lai L, Wang Q, Chen Z, . E3 ligase FBXW7 restricts M2-like tumor-associated macrophage polarization by targeting c-Myc. . 12:24394-24423. https://doi.org/10.18632/aging.202293

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                TY  - JOUR
                AU  - Zhong, Lijia 
                AU  - Zhang, Yuanyuan 
                AU  - Li, Mengyao 
                AU  - Song, Yinjing 
                AU  - Liu, Danhui 
                AU  - Yang, Xin 
                AU  - Yang, Dehua 
                AU  - Qu, Hao 
                AU  - Lai, Lihua 
                AU  - Wang, Qingqing 
                AU  - Chen, Zhimin 
                TI  - E3 ligase FBXW7 restricts M2-like tumor-associated macrophage polarization by targeting c-Myc
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202293
                DO  - 10.18632/aging.202293
                SP  - 24394
                EP  - 24423
                PY  - 
                AB  - FBXW7 functions as an E3 ubiquitin ligase to mediate oncoprotein degradation via the ubiquitin-proteasome system in cancer cells, effectively inhibiting the growth and survival of tumor cells. However, little is known about the functions of FBXW7 in macrophages and the tumor immune microenvironment. In this study, we find that FBXW7 suppresses M2-like tumor-associated macrophage (TAM) polarization to limit tumor progression. We identified a significant increase in the proportion of M2-like TAMs and aggravated tumor growth in mice with myeloid FBXW7 deficiency by subcutaneous inoculation with Lewis lung carcinoma cells (LLCs). When stimulated with LLCs supernatant in vitro, FBXW7-knockout macrophages displayed increased M2 macrophage polarization and enhanced ability of supporting cancer cells growth. In mechanism, we confirmed that FBXW7 inhibited M2-like TAM polarization by mediating c-Myc degradation via the ubiquitin-proteasome system. These findings highlight the role of FBXW7 in M2-like TAM polarization and provide new insights into the potential targets for cancer immunotherapies.
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FOXM1/DVL2/Snail axis drives metastasis and chemoresistance of colorectal cancer

Yuhan Yang, Hequn Jiang, Wanxin Li, Linyi Chen, Wanglong Zhu, Yu Xian, Zhengyu Han, Lan Yin, Yao Liu, Yi Wang, Kejian Pan, Kun Zhang,

https://doi.org/10.18632/aging.202300 pp 24424—24440

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Yang Y, Jiang H, Li W, Chen L, Zhu W, Xian Y, Han Z, Yin L, Liu Y, Wang Y, Pan K, Zhang K, . FOXM1/DVL2/Snail axis drives metastasis and chemoresistance of colorectal cancer. . 12:24424-24440. https://doi.org/10.18632/aging.202300

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                TY  - JOUR
                AU  - Yang, Yuhan 
                AU  - Jiang, Hequn 
                AU  - Li, Wanxin 
                AU  - Chen, Linyi 
                AU  - Zhu, Wanglong 
                AU  - Xian, Yu 
                AU  - Han, Zhengyu 
                AU  - Yin, Lan 
                AU  - Liu, Yao 
                AU  - Wang, Yi 
                AU  - Pan, Kejian 
                AU  - Zhang, Kun 
                TI  - FOXM1/DVL2/Snail axis drives metastasis and chemoresistance of colorectal cancer
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.202300
                DO  - 10.18632/aging.202300
                SP  - 24424
                EP  - 24440
                PY  - 
                AB  - Colorectal cancer (CRC) is the third most common type of cancer worldwide. Metastasis and chemoresistance are regarded as the two leading causes of treatment failure and high mortality in CRC. Forkhead Box M1 (FOXM1) has been involved in malignant behaviors of cancer. However, the role and mechanism of FOXM1 in simultaneously regulating metastasis and chemoresistance of CRC remain poorly understood. Here, we found that FOXM1 was overexpressed in oxaliplatin- and vincristine-resistant CRC cells (HCT-8/L-OHP and HCT-8/VCR) with enhanced metastatic potential, compared with HCT-8 cells. FOXM1 overexpression increased migration, invasion and drug-resistance to oxaliplatin and vincristine in HCT-8 cells, while FOXM1 knockdown using shFOXM1 impaired metastasis and drug-resistance in HCT-8/L-OHP and HCT-8/VCR cells. Moreover, FOXM1 up-regulated Snail to trigger epithelial-mesenchymal transition-like molecular changes and multidrug-resistance protein P-gp expression, while silencing Snail inhibited FOXM1-induced metastasis and drug-resistance. We further identified that disheveled-2 (DVL2) was crucial for FOXM1-induced Snail expression, metastasis and chemoresistance. Furthermore, FOXM1 bound to DVL2, and enhanced nuclear translocation of DVL2 and DVL2-mediated transcriptional activity of Wnt/&#x3B2;-catenin known to induce Snail expression. In conclusion, FOXM1/DVL2/Snail axis triggered aggressiveness of CRC. Blocking FOXM1/DVL2/Snail pathway simultaneously inhibited metastasis and chemoresistance in CRC cells, providing a new strategy for successful CRC treatment.
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Caloric restriction: implications for sarcopenia and potential mechanisms

Wen-Qing Xie, Wen-Feng Xiao, Kun Tang, Yu-Xiang Wu, Pei-Wu Hu, Yu-Sheng Li, Yu Duan, Shan Lv,

https://doi.org/10.18632/aging.103987 pp 24441—24452

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Xie W, Xiao W, Tang K, Wu Y, Hu P, Li Y, Duan Y, Lv S, . Caloric restriction: implications for sarcopenia and potential mechanisms. . 12:24441-24452. https://doi.org/10.18632/aging.103987

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                TY  - JOUR
                AU  - Xie, Wen-Qing 
                AU  - Xiao, Wen-Feng 
                AU  - Tang, Kun 
                AU  - Wu, Yu-Xiang 
                AU  - Hu, Pei-Wu 
                AU  - Li, Yu-Sheng 
                AU  - Duan, Yu 
                AU  - Lv, Shan 
                TI  - Caloric restriction: implications for sarcopenia and potential mechanisms
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103987
                DO  - 10.18632/aging.103987
                SP  - 24441
                EP  - 24452
                PY  - 
                AB  - Sarcopenia is a potential risk factor for weakness, disability and death in elderly individuals. Therefore, seeking effective methods to delay and treat sarcopenia and to improve the quality of life of elderly individuals is a trending topic in geriatrics. Caloric restriction (CR) is currently recognized as an effective means to extend the lifespan and delay the decline in organ function caused by aging. In this review, we describe the effects of CR on improving muscle protein synthesis, delaying muscle atrophy, regulating muscle mitochondrial function, maintaining muscle strength, promoting muscle stem cell (MuSC) regeneration and differentiation, and thus protecting against sarcopenia. We also summarize the possible cellular mechanisms by which CR delays sarcopenia. CR can delay sarcopenia by reducing the generation of oxygen free radicals, reducing oxidative stress damage, enhancing mitochondrial function, improving protein homeostasis, reducing iron overload, increasing autophagy and apoptosis, and reducing inflammation. However, the relationships between CR and genetics, sex, animal strain, regimen duration and energy intake level are complex. Therefore, further study of the proper timing and application method of CR to prevent sarcopenia is highly important for the aging population.
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COVID-19
Role of angiotensin-converting enzyme 2 in neurodegenerative diseases during the COVID-19 pandemic

Zhenyu Li, Xiaolin Xu, Meiling Yang, Jianping Feng, Cunming Liu, Chun Yang,

https://doi.org/10.18632/aging.103993 pp 24453—24461

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Li Z, Xu X, Yang M, Feng J, Liu C, Yang C, . Role of angiotensin-converting enzyme 2 in neurodegenerative diseases during the COVID-19 pandemic. . 12:24453-24461. https://doi.org/10.18632/aging.103993

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                TY  - JOUR
                AU  - Li, Zhenyu 
                AU  - Xu, Xiaolin 
                AU  - Yang, Meiling 
                AU  - Feng, Jianping 
                AU  - Liu, Cunming 
                AU  - Yang, Chun 
                TI  - Role of angiotensin-converting enzyme 2 in neurodegenerative diseases during the COVID-19 pandemic
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.103993
                DO  - 10.18632/aging.103993
                SP  - 24453
                EP  - 24461
                PY  - 
                AB  - SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) uses the angiotensin-converting enzyme 2 (ACE2) receptor for infecting and spreading in humans. Studies have shown that the widespread expression of ACE2 in human tissues may be associated with organ function damage (e.g., lung, kidney, and stomach) in patients with coronavirus disease 2019 (COVID-19). However, in neurodegenerative diseases, whose pathogenesis is closely related to advanced age, ACE2 plays a neurotrophic and protective role by activating the ACE2/Ang-(1-7)/Mas axis, thus inhibiting cognitive impairment. Early reports have revealed that the elderly are more susceptible to COVID-19 and that elderly patients with COVID-19 have faster disease progression and higher mortality. Therefore, during the COVID-19 pandemic, it is crucial to understand the role of ACE2 in neurodegenerative diseases. In this paper, we review the relationship between COVID-19, neurodegenerative diseases, and ACE2, as well as provide recommendations for the protection of elderly patients with neurodegenerative diseases during the COVID-19 pandemic.
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COVID-19
Clinical challenges in cancer patients with COVID-19: Aging, immunosuppression, and comorbidities

Lu Wang, Yinan Sun, Ye Yuan, Qi Mei, Xianglin Yuan,

https://doi.org/10.18632/aging.104205 pp 24462—24474

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Wang L, Sun Y, Yuan Y, Mei Q, Yuan X, . Clinical challenges in cancer patients with COVID-19: Aging, immunosuppression, and comorbidities. . 12:24462-24474. https://doi.org/10.18632/aging.104205

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                TY  - JOUR
                AU  - Wang, Lu 
                AU  - Sun, Yinan 
                AU  - Yuan, Ye 
                AU  - Mei, Qi 
                AU  - Yuan, Xianglin 
                TI  - Clinical challenges in cancer patients with COVID-19: Aging, immunosuppression, and comorbidities
                JO  - 
                JA  - 
                VL  - 12
                IS  - 23
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.104205
                DO  - 10.18632/aging.104205
                SP  - 24462
                EP  - 24474
                PY  - 
                AB  - COVID-19 caused by severe acute respiratory syndrome coronavirus 2 has developed into a global pandemic. COVID-19 poses a huge threat to health care, and the shortage of medical resources caused by COVID-19 brought serious secondary disasters to elderly cancer patients who are particularly dependent on medical resources. The clinical challenges of cancer management, including aging, immunosuppression, and comorbidities, make cancer patients more vulnerable to COVID-19 with different clinical manifestations, disease severity, and outcomes. The review comprehensively analyzed the characteristics of the cancer patients under the pandemic and concluded that cancer patients were more susceptible to COVID-19, and also concluded that they were more likely to develop poor outcomes and the severe form of the disease. Three basic management strategies have been proposed to protect susceptible elderly cancer patients, find reliable indicators to monitor the course of disease, and implement effective prevention measures.
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Correction for: TAp63γ influences mouse cartilage development

Qian Wang, Na Li, Fangzhou Chen, Ruoxuan Hei, Junxia Gu, Yaojuan Lu, Lichun Sun, Qiping Zheng,

https://doi.org/10.18632/aging.104221 pp 24475

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Wang Q, Li N, Chen F, Hei R, Gu J, Lu Y, Sun L, Zheng Q, . Correction for: TAp63γ influences mouse cartilage development. . 12:24475-24475. https://doi.org/10.18632/aging.104221

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Volume 12, Issue 23

About the Cover

Editorials

Volha Mezhnina, Roman Kondratov,

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Igor Shats, Xiaoling Li,

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Research Papers

COVID-19 Evolution of COVID-19 in patients with autoimmune rheumatic diseases

Rongrong Pang, Jun Zhao, Zhenhua Gan, Zhiliang Hu, Xiang Xue, Yanjun Wu, Qinghua Qiao, Aifang Zhong, Xinyi Xia, Hui Liao, Zhihua Wang, Libo Zhang,

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COVID-19 Clinical characteristics and fatal outcomes of hypertension in patients with severe COVID-19

Xiaocheng Cheng, Guoqiang Cai, Xuesong Wen, Lei Gao, Dan Jiang, Min Sun, Shu Qin, Jianzhong Zhou, Dongying Zhang,

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COVID-19 Incidence of cerebrovascular disease as a comorbidity in patients with COVID-19: A meta-analysis

Jun Zhang, Haili Wang, Min Wei, Hengzhu Zhang, Boming Xia, Xingdong Wang, Yunlong Pei, Lun Dong, Yuping Li,

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COVID-19 Risk factors for COVID-19 patients with cardiac injury: pulmonary ventilation dysfunction and oxygen inhalation insufficiency are not the direct causes

Sucheng Mu, Wei Wei, Chaoyuan Jin, Ning Pu, Kaihuan Yu, Guorong Gu, Zhe Luo, Chaoyang Tong, Yi Han,

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Anette Teo Hansen Selnø, Stephanie Schlichtner, Inna M. Yasinska, Svetlana S. Sakhnevych, Walter Fiedler, Jasmin Wellbrock, Elena Klenova, Ludmila Pavlova, Bernhard F. Gibbs, Martin Degen, Isabelle Schnyder, Nijas Aliu, Steffen M. Berger, Elizaveta Fasler-Kan, Vadim V. Sumbayev,

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Clara Sciorati, Riccardo Gamberale, Antonella Monno, Lorena Citterio, Chiara Lanzani, Rebecca De Lorenzo, Giuseppe A. Ramirez, Antonio Esposito, Paolo Manunta, Angelo A. Manfredi, Patrizia Rovere-Querini,

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Randi Chen, Brian J. Morris, Timothy A. Donlon, Kamal H. Masaki, D. Craig Willcox, Philip M.C. Davy, Richard C. Allsopp, Bradley J. Willcox,

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Kazuto Kawamura, Ichiro N. Maruyama,

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Alex Zhavoronkov, Kirill Kochetov, Peter Diamandis, Maria Mitina,

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Sergio Castañeda-Zegarra, Qindong Zhang, Amin Alirezaylavasani, Marion Fernandez-Berrocal, Rouan Yao, Valentyn Oksenych,

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Liansheng Sha, Deying Ma, Cuili Chen,

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Lianping Gou, Cheng Xue, Xiaoyan Tang, Zhiyuan Fang,

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Ya-Jen Chiu, Shu-An Lin, Wan-Ling Chen, Te-Hsien Lin, Chih-Hsin Lin, Ching-Fa Yao, Wenwei Lin, Yih-Ru Wu, Kuo-Hsuan Chang, Guey-Jen Lee-Chen, Chiung-Mei Chen,

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Bowen Wu, Yichao Gan, Ying Xu, Zhaoxing Wu, Ganyu Xu, Ping Wang, Chen Wang, Zhipeng Meng, Mengyuan Li, Jiawei Zhang, Haifeng Zhuang, Xuzhao Zhang, Linlin Yang, Jinfan Li, Xiaoxian Gan, Xiaofang Yu, Wendong Huang, Ying Gu, Rongzhen Xu,

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Kai Xu, Binshen Chen, Bingkun Li, Chaoming Li, Yiming Zhang, Ning Jiang, Bin Lang,

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Bing Zhuan, Xi Wang, Ming-Deng Wang, Zhi-Cai Li, Qun Yuan, Jun Xie, Zhao Yang,

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COVID-19
Evolution of COVID-19 in patients with autoimmune rheumatic diseases

COVID-19
Clinical characteristics and fatal outcomes of hypertension in patients with severe COVID-19

COVID-19
Incidence of cerebrovascular disease as a comorbidity in patients with COVID-19: A meta-analysis

COVID-19
Risk factors for COVID-19 patients with cardiac injury: pulmonary ventilation dysfunction and oxygen inhalation insufficiency are not the direct causes