Volume 11, Issue 2

Lu AT, Quach A, Wilson JG, Reiner AP, Aviv A, Raj K, Hou L, Baccarelli AA, Li Y, Stewart JD, Whitsel EA, Assimes TL, Ferrucci L, et al, . DNA methylation GrimAge strongly predicts lifespan and healthspan. . 11:303-327. https://doi.org/10.18632/aging.101684

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                TY  - JOUR
                AU  - Lu, Ake T. 
                AU  - Quach, Austin 
                AU  - Wilson, James G. 
                AU  - Reiner, Alex P. 
                AU  - Aviv, Abraham 
                AU  - Raj, Kenneth 
                AU  - Hou, Lifang 
                AU  - Baccarelli, Andrea A. 
                AU  - Li, Yun 
                AU  - Stewart, James D. 
                AU  - Whitsel, Eric A. 
                AU  - Assimes, Themistocles L. 
                AU  - Ferrucci, Luigi 
                AU  - Horvath, Steve 
                TI  - DNA methylation GrimAge strongly predicts lifespan and healthspan
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101684
                DO  - 10.18632/aging.101684
                SP  - 303
                EP  - 327
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Lu, Ake T. 
                AU  - Quach, Austin 
                AU  - Wilson, James G. 
                AU  - Reiner, Alex P. 
                AU  - Aviv, Abraham 
                AU  - Raj, Kenneth 
                AU  - Hou, Lifang 
                AU  - Baccarelli, Andrea A. 
                AU  - Li, Yun 
                AU  - Stewart, James D. 
                AU  - Whitsel, Eric A. 
                AU  - Assimes, Themistocles L. 
                AU  - Ferrucci, Luigi 
                AU  - Horvath, Steve 
                TI  - DNA methylation GrimAge strongly predicts lifespan and healthspan
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101684
                DO  - 10.18632/aging.101684
                SP  - 303
                EP  - 327
                PY  - 
                AB  - It was unknown whether plasma protein levels can be estimated based on DNA methylation (DNAm) levels, and if so, how the resulting surrogates can be consolidated into a powerful predictor of lifespan. We present here, seven DNAm-based estimators of plasma proteins including those of plasminogen activator inhibitor 1 (PAI-1) and growth differentiation factor 15. The resulting predictor of lifespan, DNAm GrimAge (in units of years), is a composite biomarker based on the seven DNAm surrogates and a DNAm-based estimator of smoking pack-years. Adjusting DNAm GrimAge for chronological age generated novel measure of epigenetic age acceleration, AgeAccelGrim.Using large scale validation data from thousands of individuals, we demonstrate that DNAm GrimAge stands out among existing epigenetic clocks in terms of its predictive ability for time-to-death (Cox regression P=2.0E-75), time-to-coronary heart disease (Cox P=6.2E-24), time-to-cancer (P= 1.3E-12), its strong relationship with computed tomography data for fatty liver/excess visceral fat, and age-at-menopause (P=1.6E-12). AgeAccelGrim is strongly associated with a host of age-related conditions including comorbidity count (P=3.45E-17). Similarly, age-adjusted DNAm PAI-1 levels are associated with lifespan (P=5.4E-28), comorbidity count (P= 7.3E-56) and type 2 diabetes (P=2.0E-26). These DNAm-based biomarkers show the expected relationship with lifestyle factors including healthy diet and educational attainment.Overall, these epigenetic biomarkers are expected to find many applications including human anti-aging studies.
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Impairment of hypoxia-induced angiogenesis by LDL involves a HIF-centered signaling network linking inflammatory TNFα and angiogenic VEGF

Fengyan Jin, Xiangyu Zheng, Yanping Yang, Gang Yao, Long Ye, Thorsten R. Doeppner, Dirk M. Hermann, Haifeng Wang, Yun Dai,

https://doi.org/10.18632/aging.101726 pp 328—349

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Jin F, Zheng X, Yang Y, Yao G, Ye L, Doeppner TR, Hermann DM, Wang H, Dai Y, . Impairment of hypoxia-induced angiogenesis by LDL involves a HIF-centered signaling network linking inflammatory TNFα and angiogenic VEGF. . 11:328-349. https://doi.org/10.18632/aging.101726

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                TY  - JOUR
                AU  - Jin, Fengyan 
                AU  - Zheng, Xiangyu 
                AU  - Yang, Yanping 
                AU  - Yao, Gang 
                AU  - Ye, Long 
                AU  - Doeppner, Thorsten R. 
                AU  - Hermann, Dirk M. 
                AU  - Wang, Haifeng 
                AU  - Dai, Yun 
                TI  - Impairment of hypoxia-induced angiogenesis by LDL involves a HIF-centered signaling network linking inflammatory TNFα and angiogenic VEGF
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101726
                DO  - 10.18632/aging.101726
                SP  - 328
                EP  - 349
                PY  - 
                AB  - Hypoxia inducible factors (HIFs) mediate angiogenesis via up-regulation of various pro-angiogenic factors (particularly VEGF) in response to hypoxia. Here, we report that hypoxia unexpectedly induced robust production of the pro-inflammatory factor TNFα by endothelial cells (ECs), suggesting an autocrine loop that in turn activated HIFs via an NF-κB-dependent process, resulting in production of VEGF and thereby promotion of angiogenesis. In contrast, low-density lipoprotein (LDL) prevented expression of HIFs in ECs exposed to either hypoxia or TNFα, while knockdown of either HIF-1α or HIF-2α strikingly attenuated hypoxia-induced production of VEGF by ECs as well as EC colony formation and tube formation. Significantly, LDL attenuated hypoxia-induced angiogenesis by disrupting the TNFα/NF-κB/HIF/VEGF signaling cascade via down-regulation of the TNF receptor TNF-R1, rather than TNFα itself, and multiple key components of both canonical and non-canonical NF-κB pathways. By doing so, LDL was able to either inhibit or down-regulate a wide spectrum of HIF-dependent pro-angiogenic downstream targets and signals. Together, these findings argue existence of a self-regulatory TNFα/NF-κB/HIF/VEGF signaling network in ECs, which mediates and fine-tones angiogenesis, at least in response to hypoxia. They also suggest that LDL impairs angiogenesis by disrupting this network, which might represent a novel mechanism underlying anti-angiogenic property of LDL.
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BCL2L10/BECN1 modulates hepatoma cells autophagy by regulating PI3K/AKT signaling pathway

Jiafa He, Li Deng, Heping Liu, Taiying Chen, Shengying Chen, Shangzhou Xia, Yubin Liu,

https://doi.org/10.18632/aging.101737 pp 350—370

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He J, Deng L, Liu H, Chen T, Chen S, Xia S, Liu Y, . BCL2L10/BECN1 modulates hepatoma cells autophagy by regulating PI3K/AKT signaling pathway. . 11:350-370. https://doi.org/10.18632/aging.101737

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Provider: 
 TY - JOUR
 AU - He, Jiafa 
 AU - Deng, Li 
 AU - Liu, Heping 
 AU - Chen, Taiying 
 AU - Chen, Shengying 
 AU - Xia, Shangzhou 
 AU - Liu, Yubin 
 TI - BCL2L10/BECN1 modulates hepatoma cells autophagy by regulating PI3K/AKT signaling pathway
 JO - 
 JA - 
 VL - 11
 IS - 2
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101737
 DO - 10.18632/aging.101737
 SP - 350
 EP - 370
 PY - 
 AB - The aim of this study was to investigate BCL2L10 and BECN1 expression and their effect on autophagy in hepatocellular carcinoma (HCC). We found that BCL2L10 expression was low in hepatoma tissues and cells. Overexpression of BCL2L10 decreased the activity of hepatoma cells. To analyze autophagic flux, we monitored the formation of autophagic vesicles by fluorescence protein method. Autophagy-related protein LC3B-II was accumulated and P62 was decreased, which indicated that autophagy was induced by BECN1, while BCL2L10 could suppress this trend. Immunofluorescence assay showed that BCL2L10 and Beclin 1 were co-located in hepatoma cells. Immunoprecipitation showed that BCL2L10 could inhibit the autophagy of hepatoma cells by combining with Beclin 1. ELISA and co-immunoprecipitation suggested that the combination between BCL2L10 and Beclin 1 reduced the bond between Beclin 1 and PI3KC3. Based on Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, the PI3K/AKT signaling pathway was significantly upregulated in HCC. In conclusions, BCL2L10 had a low expression in HCC tissues and cells, which could release BECN1 to induce autophagy of hepatoma cells by downregulating PI3K/AKT signaling pathway.
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Age-related alterations in the modulation of intracortical inhibition during stopping of actions

Lize Hermans, Celine Maes, Lisa Pauwels, Koen Cuypers, Kirstin-Friederike Heise, Stephan P. Swinnen, Inge Leunissen,

https://doi.org/10.18632/aging.101741 pp 371—385

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Hermans L, Maes C, Pauwels L, Cuypers K, Heise K, Swinnen SP, Leunissen I, . Age-related alterations in the modulation of intracortical inhibition during stopping of actions. . 11:371-385. https://doi.org/10.18632/aging.101741

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                TY  - JOUR
                AU  - Hermans, Lize 
                AU  - Maes, Celine 
                AU  - Pauwels, Lisa 
                AU  - Cuypers, Koen 
                AU  - Heise, Kirstin-Friederike 
                AU  - Swinnen, Stephan P. 
                AU  - Leunissen, Inge 
                TI  - Age-related alterations in the modulation of intracortical inhibition during stopping of actions
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101741
                DO  - 10.18632/aging.101741
                SP  - 371
                EP  - 385
                PY  - 
                AB  - We investigated the effect of age on the ability to modulate GABAA-ergic and GABAB-ergic inhibitory activity during stopping of action (reactive inhibition) and preparation to stop (proactive inhibition). Twenty-five young and twenty-nine older adults performed an anticipated response version of the stop-signal task with varying levels of stop-signal probability. Paired-pulse transcranial magnetic stimulation was applied to left primary motor cortex to assess the modulation of GABAA-mediated short-interval intracortical inhibition (SICI) during stopping and GABAB-mediated long-interval intracortical inhibition (LICI) during the anticipation of a stop-signal. At the behavioral level, reactive inhibition was affected by aging as indicated by longer stop-signal reaction times in older compared to young adults. In contrast, proactive inhibition was preserved at older age as both groups slowed down their go response to a similar degree with increasing stop-signal probability. At the neural level, the amount of SICI was higher in successful stop relative to go trials in young but not in older adults. LICI at the start of the trial was modulated as a function of stop-signal probability in both young and older adults. Our results suggest that specifically the recruitment of GABAA-mediated intracortical inhibition during stopping of action is affected by aging.
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Loss of GPR109A/HCAR2 induces aging-associated hepatic steatosis

Ravirajsinh N. Jadeja, Malita A. Jones, Ollya Fromal, Folami L. Powell, Sandeep Khurana, Nagendra Singh, Pamela M. Martin,

https://doi.org/10.18632/aging.101743 pp 386—400

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Jadeja RN, Jones MA, Fromal O, Powell FL, Khurana S, Singh N, Martin PM, . Loss of GPR109A/HCAR2 induces aging-associated hepatic steatosis. . 11:386-400. https://doi.org/10.18632/aging.101743

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                TY  - JOUR
                AU  - Jadeja, Ravirajsinh N. 
                AU  - Jones, Malita A. 
                AU  - Fromal, Ollya 
                AU  - Powell, Folami L. 
                AU  - Khurana, Sandeep 
                AU  - Singh, Nagendra 
                AU  - Martin, Pamela M. 
                TI  - Loss of GPR109A/HCAR2 induces aging-associated hepatic steatosis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101743
                DO  - 10.18632/aging.101743
                SP  - 386
                EP  - 400
                PY  - 
                AB  - GPR109A agonists have been used for the treatment of obesity however, the role of GPR109A in regulating aging-associated alterations in lipid metabolism is unknown. In this study we used Gpr109a-/- mice to investigate the effect of aging in the regulation of lipid accumulation. We observed that in mouse and human livers, in addition to Kupffer cells, GPR109A is expressed in hepatocytes. Over 12 months, compared to wild type (WT), Gpr109a-/- mice gained significantly more weight. Food intake and levels of serum lipids were similar among both groups. Compared to age-matched WT mice, 12-months old Gpr109a-/- mice had significantly increased liver weight, hepatic steatosis and serum markers of liver injury. The fatty liver phenotype in Gpr109a-/- mice was associated with increased hepatic expression of lipogenesis genes and decreased expression of lipolysis genes. Gpr109a-/- mice had significantly increased fat tissues, which was associated with significant increase in adipocyte diameter and surface area. Adipose tissue from Gpr109a-/- mice had increased expression of lipogenesis genes; however, expression of lipolytic genes was similar in both groups. Collectively, these results indicate that during aging, GPR109A modulates de novo lipid accumulation in liver and adipose tissue, and its dysregulation can lead to age-associated obesity and hepatic steatosis.
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3,4,5-Tricaffeoylquinic acid induces adult neurogenesis and improves deficit of learning and memory in aging model senescence-accelerated prone 8 mice

Kazunori Sasaki, Julie Davies, Noelia Geribaldi Doldán, Sayo Arao, Farhana Ferdousi, Francis G. Szele, Hiroko Isoda,

https://doi.org/10.18632/aging.101748 pp 401—422

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Sasaki K, Davies J, Doldán NG, Arao S, Ferdousi F, Szele FG, Isoda H, . 3,4,5-Tricaffeoylquinic acid induces adult neurogenesis and improves deficit of learning and memory in aging model senescence-accelerated prone 8 mice. . 11:401-422. https://doi.org/10.18632/aging.101748

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                TY  - JOUR
                AU  - Sasaki, Kazunori 
                AU  - Davies, Julie 
                AU  - Doldán, Noelia Geribaldi 
                AU  - Arao, Sayo 
                AU  - Ferdousi, Farhana 
                AU  - Szele, Francis G. 
                AU  - Isoda, Hiroko 
                TI  - 3,4,5-Tricaffeoylquinic acid induces adult neurogenesis and improves deficit of learning and memory in aging model senescence-accelerated prone 8 mice
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101748
                DO  - 10.18632/aging.101748
                SP  - 401
                EP  - 422
                PY  - 
                AB  - Caffeoylquinic acid (CQA) is a natural polyphenol with evidence of antioxidant and neuroprotective effects and prevention of deficits in spatial learning and memory. We studied the cognitive-enhancing effect of 3,4,5-tricaffeoylquinic acid (TCQA) and explored its cellular and molecular mechanism in the senescence-accelerated mouse prone 8 (SAMP8) model of aging and Alzheimer’s disease as well as in human neural stem cells (hNSCs). Mice were fed with 5 mg/kg of TCQA for 30 days and were tested in the Morris water maze (MWM). Brain tissues were collected for immunohistochemical detection of bromodeoxyuridine (BrdU) to detect activated stem cells and newborn neurons. TCQA-treated SAMP8 exhibited significantly improved cognitive performance in MWM compared to water-treated SAMP8. TCQA-treated SAMP8 mice also had significantly higher numbers of BrdU+/glial fibrillary acidic protein (GFAP+) and BrdU+/Neuronal nuclei (NeuN+) cells in the dentate gyrus (DG) neurogenic niche compared with untreated SAMP8. In hNSCs, TCQA induced cell cycle arrest at G0/G1, actin cytoskeleton organization, chromatin remodeling, neuronal differentiation, and bone morphogenetic protein signaling. The neurogenesis promoting effect of TCQA in the DG of SAMP8 mice might explain the cognition-enhancing influence of TCQA observed in our study, and our hNSCs in aggregate suggest a therapeutic potential for TCQA in aging-associated diseases.
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Expression and gene regulation network of RBM8A in hepatocellular carcinoma based on data mining

Yan Lin, Rong Liang, Yufen Qiu, Yufeng Lv, Jinyan Zhang, Gang Qin, Chunling Yuan, Zhihui Liu, Yongqiang Li, Donghua Zou, Yingwei Mao,

https://doi.org/10.18632/aging.101749 pp 423—447

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Lin Y, Liang R, Qiu Y, Lv Y, Zhang J, Qin G, Yuan C, Liu Z, Li Y, Zou D, Mao Y, . Expression and gene regulation network of RBM8A in hepatocellular carcinoma based on data mining. . 11:423-447. https://doi.org/10.18632/aging.101749

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Provider: 
 TY - JOUR
 AU - Lin, Yan 
 AU - Liang, Rong 
 AU - Qiu, Yufen 
 AU - Lv, Yufeng 
 AU - Zhang, Jinyan 
 AU - Qin, Gang 
 AU - Yuan, Chunling 
 AU - Liu, Zhihui 
 AU - Li, Yongqiang 
 AU - Zou, Donghua 
 AU - Mao, Yingwei 
 TI - Expression and gene regulation network of RBM8A in hepatocellular carcinoma based on data mining
 JO - 
 JA - 
 VL - 11
 IS - 2
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101749
 DO - 10.18632/aging.101749
 SP - 423
 EP - 447
 PY - 
 AB - RNA binding motif protein 8A (RBM8A) is an RNA binding protein in a core component of the exon junction complex. Abnormal RBM8A expression is associated with carcinogenesis. We used sequencing data from the Cancer Genome Atlas database and Gene Expression Omnibus, analyzed RBM8A expression and gene regulation networks in hepatocellular carcinoma (HCC). Expression was analyzed using OncomineTM and Gene Expression Profiling Interactive Analysis tools, while RBM8A alterations and related functional networks were identified using cBioPortal. LinkedOmics was used to identify differential gene expression with RBM8A and to analyze Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathways. Gene enrichment analysis examined target networks of kinases, miRNAs and transcription factors. We found that RBM8A is overexpressed and the RBM8A gene often amplified in HCC. Expression of this gene is linked to functional networks involving the ribosome and RNA metabolic signaling pathways. Functional network analysis suggested that RBM8A regulates the spliceosome, ribosome, DNA replication and cell cycle signaling via pathways involving several cancer-related kinases, miRNAs and E2F Transcription Factor 1. Our results demonstrate that data mining efficiently reveals information about RBM8A expression and potential regulatory networks in HCC, laying a foundation for further study of the role of RBM8A in carcinogenesis.
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miRNA-mRNA crosstalk in myocardial ischemia induced by calcified aortic valve stenosis

Chenyang Duan, Zhezhe Cao, Fuqin Tang, Zhao Jian, Chunshui Liang, Hong Liu, Yingbin Xiao, Liangming Liu, Ruiyan Ma,

https://doi.org/10.18632/aging.101751 pp 448—466

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Duan C, Cao Z, Tang F, Jian Z, Liang C, Liu H, Xiao Y, Liu L, Ma R, . miRNA-mRNA crosstalk in myocardial ischemia induced by calcified aortic valve stenosis. . 11:448-466. https://doi.org/10.18632/aging.101751

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                TY  - JOUR
                AU  - Duan, Chenyang 
                AU  - Cao, Zhezhe 
                AU  - Tang, Fuqin 
                AU  - Jian, Zhao 
                AU  - Liang, Chunshui 
                AU  - Liu, Hong 
                AU  - Xiao, Yingbin 
                AU  - Liu, Liangming 
                AU  - Ma, Ruiyan 
                TI  - miRNA-mRNA crosstalk in myocardial ischemia induced by calcified aortic valve stenosis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101751
                DO  - 10.18632/aging.101751
                SP  - 448
                EP  - 466
                PY  - 
                AB  - Aortic valve stenosis is the most common cause of morbidity and mortality in valvular heart disease in aged people. Both microRNA (miRNA) and mRNA are potential targets for the diagnosis and therapeutic intervention of myocardial ischemia induced by calcified aortic valve stenosis (CAVS), with unclear mechanisms. Here, 3 gene expression profiles of 47 male participants were applied to generate shared differentially expressed genes (DEGs) with significant major biological functions. Moreover, 20 hub genes were generated by a Weighted Genes Co-Expression Network Analysis (WGCNA) and were cross-linked to miRNA based on miRanda/miRwalk2 databases. Integrated miRNA/mRNA analysis identified several novel miRNAs and targeted genes as diagnostic/prognostic biomarkers or therapeutic targets in CAVS patients. In addition, the clinical data suggested that myocardial hypertrophy and myocardial ischemia in CAVS patients are likely associated with hub genes and the upstream regulatory miRNAs. Together, our data provide evidence that miRNAs and their targeted genes play an important role in the pathogenesis of myocardial hypertrophy and ischemia in patients with CAVS.
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Combined eight-long noncoding RNA signature: a new risk score predicting prognosis in elderly non-small cell lung cancer patients

Runchen Miao, Cuiyun Ge, Xing Zhang, Yang He, Xiaohua Ma, Xiaohong Xiang, Jingxian Gu, Yunong Fu, Kai Qu, Chang Liu, Qifei Wu, Ting Lin,

https://doi.org/10.18632/aging.101752 pp 467—479

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Miao R, Ge C, Zhang X, He Y, Ma X, Xiang X, Gu J, Fu Y, Qu K, Liu C, Wu Q, Lin T, . Combined eight-long noncoding RNA signature: a new risk score predicting prognosis in elderly non-small cell lung cancer patients. . 11:467-479. https://doi.org/10.18632/aging.101752

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                TY  - JOUR
                AU  - Miao, Runchen 
                AU  - Ge, Cuiyun 
                AU  - Zhang, Xing 
                AU  - He, Yang 
                AU  - Ma, Xiaohua 
                AU  - Xiang, Xiaohong 
                AU  - Gu, Jingxian 
                AU  - Fu, Yunong 
                AU  - Qu, Kai 
                AU  - Liu, Chang 
                AU  - Wu, Qifei 
                AU  - Lin, Ting 
                TI  - Combined eight-long noncoding RNA signature: a new risk score predicting prognosis in elderly non-small cell lung cancer patients
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101752
                DO  - 10.18632/aging.101752
                SP  - 467
                EP  - 479
                PY  - 
                AB  - The elderly are the majority of patients with non-small cell lung cancer (NSCLC). Compared to the overall population's predictive guidance, an effective predictive guidance for elderly patients can better guide patients' postoperative treatment and improve overall survival (OS) and disease-free survival (DFS). Recently, the long non-coding RNAs (lncRNAs) have been found to play an important role in predicting tumor prognosis. To identify potential lncRNAs to predict survival in elderly patients with NSCLC, in the present study, we chose 456 elderly patients with NSCLC and analyzed differentially expressed lncRNAs from four Gene Expression Omnibus (GEO) datasets (GSE30219, GSE31546, GSE37745 and GSE50081). We then constructed an eight-lncRNA formula to predict elderly patients’ prognosis in NSCLC. Furthermore, we validated the prognostic values of the new risk model in two independent datasets, TCGA (n=670) and GSE31210 (n=130). Our data suggested a significant association between risk model and patients’ prognosis. Finally, stratification analysis further revealed the eight-lncRNA signature was an independent factor to predict OS and DFS in stage I elderly patients from both the discovery and validation groups. Functional prediction revealed that 8 lncRNAs have potential effects on tumor immune processes such as lymphocyte activation and TNF production in NSCLC. In summary, our data provides evidence that the eight-lncRNA signature could serve as an independent biomarker to predict prognosis in elderly patients with NSCLC especially in elderly stage I patients.
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Development of a prognostic index based on an immunogenomic landscape analysis of papillary thyroid cancer

Peng Lin, Yi-nan Guo, Lin Shi, Xiao-jiao Li, Hong Yang, Yun He, Qing Li, Yi-wu Dang, Kang-lai Wei, Gang Chen,

https://doi.org/10.18632/aging.101754 pp 480—500

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Lin P, Guo Y, Shi L, Li X, Yang H, He Y, Li Q, Dang Y, Wei K, Chen G, . Development of a prognostic index based on an immunogenomic landscape analysis of papillary thyroid cancer. . 11:480-500. https://doi.org/10.18632/aging.101754

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                TY  - JOUR
                AU  - Lin, Peng 
                AU  - Guo, Yi-nan 
                AU  - Shi, Lin 
                AU  - Li, Xiao-jiao 
                AU  - Yang, Hong 
                AU  - He, Yun 
                AU  - Li, Qing 
                AU  - Dang, Yi-wu 
                AU  - Wei, Kang-lai 
                AU  - Chen, Gang 
                TI  - Development of a prognostic index based on an immunogenomic landscape analysis of papillary thyroid cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101754
                DO  - 10.18632/aging.101754
                SP  - 480
                EP  - 500
                PY  - 
                AB  - Background: Papillary thyroid cancer (PTC) is the most common subtype of thyroid cancer, and inflammation relates significantly to its initiation and prognosis. Systematic exploration of the immunogenomic landscape therein to assist in PTC prognosis is therefore urgent. The Cancer Genome Atlas (TCGA) project provides a large number of genetic PTC samples that enable a comprehensive and reliable immunogenomic study.Methods: We integrated the expression profiles of immune-related genes (IRGs) and progression-free intervals (PFIs) in survival in 493 PTC patients based on the TCGA dataset. Differentially-expressed and survival-associated IRGs in PTC patients were estimated a computational difference algorithm and COX regression analysis. The potential molecular mechanisms and properties of these PTC-specific IRGs were also explored with the help of computational biology. A new prognostic index based on immune-related genes was developed by using multivariable COX analysis.Results: A total of 46 differentially expressed immune-related genes were significantly correlated with clinical outcome of PTC patients. Functional enrichment analysis revealed that these genes were actively involved in a cytokine-cytokine receptor interaction KEGG pathway. A prognostic signature based on RGs (AGTR1, CTGF, FAM3B, IL11, IL17C, PTH2R and SPAG11A) performed moderately in prognostic predictions and correlated with age, tumor stage, metastasis, number of lesions, and tumor burden. Intriguingly, the prognostic index based on IRGs reflected infiltration by several types of immune cells.Conclusions: Together, our results screened several IRGs of clinical significance, revealed drivers of the immune repertoire, and demonstrated the importance of a personalized, IRG-based immune signature in the recognition, surveillance, and prognosis of PTC.
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Prognostic value of immune checkpoint molecules in head and neck cancer: a meta-analysis

Yi-Qun Jia, Bo Yang, Li-Ling Wen, Wen-Xin Mu, Zhi Wang, Bin Cheng,

https://doi.org/10.18632/aging.101756 pp 501—522

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Jia Y, Yang B, Wen L, Mu W, Wang Z, Cheng B, . Prognostic value of immune checkpoint molecules in head and neck cancer: a meta-analysis. . 11:501-522. https://doi.org/10.18632/aging.101756

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                TY  - JOUR
                AU  - Jia, Yi-Qun 
                AU  - Yang, Bo 
                AU  - Wen, Li-Ling 
                AU  - Mu, Wen-Xin 
                AU  - Wang, Zhi 
                AU  - Cheng, Bin 
                TI  - Prognostic value of immune checkpoint molecules in head and neck cancer: a meta-analysis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101756
                DO  - 10.18632/aging.101756
                SP  - 501
                EP  - 522
                PY  - 
                AB  - Immune checkpoint molecules are important targets in cancer immunotherapy, but their association with prognosis in patients with head and neck cancer is controversial. In this meta-analysis, we searched for 12 immune checkpoint molecules in the PubMed, Embase and Cochrane Library databases and retrieved 52 studies with 7127 participants. Among the molecules included in the search, indoleamine 2, 3-dioxygenase (IDO), programmed death ligand 1 (PD-L1), and programmed death 1 (PD-1) met the inclusion criteria for further analysis. Higher expression of IDO was associated with poorer overall survival in head and neck cancer patients (P = 0.011), but higher expression of PD-L1 correlated with better overall survival specifically in nasopharyngeal carcinoma patients (P = 0.01). In a sensitivity analysis, higher PD-L1 expression correlated with better progression-free survival (P = 0.043), and was associated with better overall survival in Caucasian subjects (P = 0.02), nasopharyngeal carcinoma patients (P = 0.015), and studies with small sample sizes (P = 0.001). PD-1 had no prognostic significance. There was no publication bias affecting the results. Thus, among the immune checkpoint molecules, IDO and PD-L1 are potential prognostic predictors in head and neck cancer.
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lncRNA-ES3/miR-34c-5p/BMF axis is involved in regulating high-glucose-induced calcification/senescence of VSMCs

Xiao Lin, Jun-Kun Zhan, Jia-Yu Zhong, Yan-Jiao Wang, Yi Wang, Shuang Li, Jie-Yu He, Pan Tan, Yi-Yin Chen, Xue-Bin Liu, Xing-Jun Cui, You-Shuo Liu,

https://doi.org/10.18632/aging.101758 pp 523—535

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Lin X, Zhan J, Zhong J, Wang Y, Wang Y, Li S, He J, Tan P, Chen Y, Liu X, Cui X, Liu Y, . lncRNA-ES3/miR-34c-5p/BMF axis is involved in regulating high-glucose-induced calcification/senescence of VSMCs. . 11:523-535. https://doi.org/10.18632/aging.101758

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                TY  - JOUR
                AU  - Lin, Xiao 
                AU  - Zhan, Jun-Kun 
                AU  - Zhong, Jia-Yu 
                AU  - Wang, Yan-Jiao 
                AU  - Wang, Yi 
                AU  - Li, Shuang 
                AU  - He, Jie-Yu 
                AU  - Tan, Pan 
                AU  - Chen, Yi-Yin 
                AU  - Liu, Xue-Bin 
                AU  - Cui, Xing-Jun 
                AU  - Liu, You-Shuo 
                TI  - lncRNA-ES3/miR-34c-5p/BMF axis is involved in regulating high-glucose-induced calcification/senescence of VSMCs
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101758
                DO  - 10.18632/aging.101758
                SP  - 523
                EP  - 535
                PY  - 
                AB  - Vascular calcification/aging is common in diabetes and is associated with increased morbidity and mortality of patients. MiR-34c-5p, not miR-34c-3p, was suppressed significantly in calcification/senescence of human aorta vascular smooth muscle cells (HA-VSMCs) induced by high glucose, which was proven by the formation of mineralized nodules and staining of senescence associated-β-galactosidase staining (SA β-gal) positive cells. Overexpression of miR-34c-5p alleviated calcification/senescence of HA-VSMCs, whereas inhibition of miR-34c-5p received the opposite results. Bcl-2 modifying factor (BMF) was a functional target of miR-34c-5p and it was involved in the process of calcification/senescence of HA-VSMCs. Besides, lncRNA-ES3 acted as a competing endogenous RNAs (ceRNA) of miR-34c-5p to enhance BMF expression. Further, lncRNA-ES3 inhibited miR-34c-5p expression by direct interaction and its knockdown suppressed the calcification/senescence of HA-VSMCs. Our results showed for the first time that the calcification/senescence of VSMCs was regulated by lncRNA-ES3 /miR-34c-5p/BMF axis.
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Geniposide-mediated protection against amyloid deposition and behavioral impairment correlates with downregulation of mTOR signaling and enhanced autophagy in a mouse model of Alzheimer's disease

Zhihua Zhang, Xiaojian Wang, Di Zhang, Yueze Liu, Lin Li,

https://doi.org/10.18632/aging.101759 pp 536—548

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Zhang Z, Wang X, Zhang D, Liu Y, Li L, . Geniposide-mediated protection against amyloid deposition and behavioral impairment correlates with downregulation of mTOR signaling and enhanced autophagy in a mouse model of Alzheimer's disease. . 11:536-548. https://doi.org/10.18632/aging.101759

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                TY  - JOUR
                AU  - Zhang, Zhihua 
                AU  - Wang, Xiaojian 
                AU  - Zhang, Di 
                AU  - Liu, Yueze 
                AU  - Li, Lin 
                TI  - Geniposide-mediated protection against amyloid deposition and behavioral impairment correlates with downregulation of mTOR signaling and enhanced autophagy in a mouse model of Alzheimer's disease
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101759
                DO  - 10.18632/aging.101759
                SP  - 536
                EP  - 548
                PY  - 
                AB  - Geniposide, an iridoid glycoside extract from the gardenia fruit, is used in traditional Chinese medicine to alleviate symptoms of liver and inflammatory diseases. Geniposide activates GLP-1 receptors, known to modulate the activity of mechanistic target of rapamycin (mTOR), a key kinase regulating energy balance, proliferation, and survival in cells. mTOR activation inhibits autophagy, which is often disrupted in age-related diseases. Modulation of mTOR function to increase autophagy and inhibit apoptosis is involved in the protective effects of pharmacologic agents targeting diabetes and Alzheimer’s disease (AD). We investigated whether such mechanism could mediate geniposide’s neuroprotective effects in the APP/PS1 mouse model of AD. Eight-week treatment with geniposide improved cognitive scores in behavioral tests, reduced amyloid-β 1-40 plaque deposition, and reduced soluble Aβ1-40 and Aβ1-42 levels in the APP/PS1 mouse brain.This also showed increased p-Akt/Akt, p-mTOR/mTOR and decreased p-4E-BP1/4E-BP1 expression, and these patterns were partially reversed by geniposide. Evidence for enhanced autophagy, denoted by increased expression of LC3-II and Beclin1, was also seen after treatment with geniposide. Our data suggests that down regulation of mTOR signaling, leading to enhanced autophagy and lysosomal clearance of Aβ fibrils, underlies the beneficial effects of geniposide against neuropathological damage and cognitive deficits characteristic of AD.
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S100A13 promotes senescence-associated secretory phenotype and cellular senescence via modulation of non-classical secretion of IL-1α

Yuanyuan Su, Chenzhong Xu, Zhaomeng Sun, Yao Liang, Guodong Li, Tanjun Tong, Jun Chen,

https://doi.org/10.18632/aging.101760 pp 549—572

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Su Y, Xu C, Sun Z, Liang Y, Li G, Tong T, Chen J, . S100A13 promotes senescence-associated secretory phenotype and cellular senescence via modulation of non-classical secretion of IL-1α. . 11:549-572. https://doi.org/10.18632/aging.101760

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                TY  - JOUR
                AU  - Su, Yuanyuan 
                AU  - Xu, Chenzhong 
                AU  - Sun, Zhaomeng 
                AU  - Liang, Yao 
                AU  - Li, Guodong 
                AU  - Tong, Tanjun 
                AU  - Chen, Jun 
                TI  - S100A13 promotes senescence-associated secretory phenotype and cellular senescence via modulation of non-classical secretion of IL-1α
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101760
                DO  - 10.18632/aging.101760
                SP  - 549
                EP  - 572
                PY  - 
                AB  - Senescent cells display the senescence-associated secretory phenotype (SASP) which plays important roles in cancer, aging, etc. Cell surface-bound IL-1α is a crucial SASP factor and acts as an upstream regulator to induce NF-κB activity and subsequent SASP genes transcription. IL-1α exports to cell surface via S100A13 protein-dependent non-classical secretory pathway. However, the status of this secretory pathway during cellular senescence and its role in cellular senescence remain unknown. Here, we show that S100A13 is up-regulated in various types of cellular senescence. S100A13 overexpression increases cell surface-associated IL-1α level, NF-κB activity and subsequent multiple SASP genes induction, whereas S100A13 knockdown has an opposite role. We also exhibit that Cu2+ level is elevated during cellular senescence. Lowering Cu2+ level decreases cell surface-bound IL-1α level, NF-κB activity and SASP production. Moreover, S100A13 overexpression promotes oncogene Ras-induced cell senescence (Ras OIS), Doxorubicin-induced cancer cell senescence (TIS) and replicative senescence, while impairment of non-classical secretory pathway of IL-1α delays cellular senescence. In addition, intervention of S100A13 affects multiple SASP and cellular senescence mediators including p38, γ-H2AX, and mTORC1. Taken together, our findings unveil a critical role of the non-classical secretory pathway of IL-1α in cellular senescence and SASP regulation.
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Anti-senescence role of heterozygous fumarate hydratase gene knockout in rat lung fibroblasts in vitro

Zhirui Fan, Lifeng Li, Xiaoli Li, Meng Zhang, Mengmeng Dou, Jing Zhao, Jing Cao, Xiaoming Deng, Mingzhi Zhang, Huixiang Li, Zhenhe Suo,

https://doi.org/10.18632/aging.101761 pp 573—589

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Fan Z, Li L, Li X, Zhang M, Dou M, Zhao J, Cao J, Deng X, Zhang M, Li H, Suo Z, . Anti-senescence role of heterozygous fumarate hydratase gene knockout in rat lung fibroblasts in vitro. . 11:573-589. https://doi.org/10.18632/aging.101761

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Provider: 
 TY - JOUR
 AU - Fan, Zhirui 
 AU - Li, Lifeng 
 AU - Li, Xiaoli 
 AU - Zhang, Meng 
 AU - Dou, Mengmeng 
 AU - Zhao, Jing 
 AU - Cao, Jing 
 AU - Deng, Xiaoming 
 AU - Zhang, Mingzhi 
 AU - Li, Huixiang 
 AU - Suo, Zhenhe 
 TI - Anti-senescence role of heterozygous fumarate hydratase gene knockout in rat lung fibroblasts in vitro
 JO - 
 JA - 
 VL - 11
 IS - 2
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101761
 DO - 10.18632/aging.101761
 SP - 573
 EP - 589
 PY - 
 AB - Abnormalities in tricarboxylic acid (TCA) cycle function were related to a variety of pathological processes. Fumarate hydratase (FH) is a required enzyme in the TCA cycle. To explore the general influence of FH knockout, we isolated FH+/– rat and normal rat lung fibroblasts and cultured these cells in vitro. The isolated fibroblasts with the current method were rather homogeneous and were confirmed spindle in morphology, positive for vimentin and negative for α-SMA (α-smooth muscle actin). Sequencing of the PCR (polymerase chain reaction) products flanking the FH gene mutation verified the FH+/– status, and the FH gene and protein expression were confirmed to be reduced in the FH+/– cells. No sign of ageing for the FH+/– cells after 61 passages was observed, but the controls died out at this stage. Flow cytometry revealed increased S-phase and decreased G1/G0 proportions with significantly less early apoptosis in FH+/– cells compared to that in control cells. At the same time, increased glucose consumption, intracellular fumarate production and extracellular lactate secretion were verified in the FH+/– cells. Correspondingly, FH+/– cells showed a lower basal oxygen consumption rate (OCR) but a higher level of reactive oxygen species (ROS) production. Single cell cloning and cell line establishment were successfully performed with the FH+/– cells at the 84th passage. All the above results indicate an important role for FH+/– in the longevity or immortality of the FH+/– cells, in which increased p53 and TERT (telomerase reverse transcriptase) protein expression, decreased p21 and p16 protein expression and negative SA-β-Gal (senescence-associated beta-galactosidase) were verified along with metabolic reprogramming.
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Relationship between senescence in macaques and bone marrow mesenchymal stem cells and the molecular mechanism

Xing-hua Pan, Yu-hao Chen, Yu-kun Yang, Xue-juan Zhang, Qing-keng Lin, Zi-an Li, Xue-min Cai, Rong-qing Pang, Xiang-qing Zhu, Guang-ping Ruan,

https://doi.org/10.18632/aging.101762 pp 590—614

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Pan X, Chen Y, Yang Y, Zhang X, Lin Q, Li Z, Cai X, Pang R, Zhu X, Ruan G, . Relationship between senescence in macaques and bone marrow mesenchymal stem cells and the molecular mechanism. . 11:590-614. https://doi.org/10.18632/aging.101762

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                TY  - JOUR
                AU  - Pan, Xing-hua 
                AU  - Chen, Yu-hao 
                AU  - Yang, Yu-kun 
                AU  - Zhang, Xue-juan 
                AU  - Lin, Qing-keng 
                AU  - Li, Zi-an 
                AU  - Cai, Xue-min 
                AU  - Pang, Rong-qing 
                AU  - Zhu, Xiang-qing 
                AU  - Ruan, Guang-ping 
                TI  - Relationship between senescence in macaques and bone marrow mesenchymal stem cells and the molecular mechanism
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101762
                DO  - 10.18632/aging.101762
                SP  - 590
                EP  - 614
                PY  - 
                AB  - The relationship between bone marrow mesenchymal stem cells (BMSCs) and aging, as well as the antiaging effects of BMSCs, was observed. An aging macaque BMSC model was established. We isolated BMSCs from young and aged macaques and used RT-PCR and Western blot to confirm the aging-related mRNAs and their expression, revealing that TERT, SIRT1 and SIRT6 expression was decreased in the aged BMSCs. The morphology, immunophenotype, differentiation potential, proliferation potential, and antiaging effects of aged and young BMSCs on 293T cells were compared. The expression of aging-related genes and the difference between the secreted cytokines in natural aging and induced aging BMSCs were observed. The transcriptome of peripheral blood mononuclear cells from macaques was analyzed by high-throughput sequencing. Finally, the transcriptional characteristics and regulatory mechanisms of gene transcription in aging macaques were investigated.
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MiR-223-3p promotes cell proliferation and metastasis by downregulating SLC4A4 in clear cell renal cell carcinoma

Wen Xiao, Xuegang Wang, Tao Wang, Jinchun Xing,

https://doi.org/10.18632/aging.101763 pp 615—633

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Xiao W, Wang X, Wang T, Xing J, . MiR-223-3p promotes cell proliferation and metastasis by downregulating SLC4A4 in clear cell renal cell carcinoma. . 11:615-633. https://doi.org/10.18632/aging.101763

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                TY  - JOUR
                AU  - Xiao, Wen 
                AU  - Wang, Xuegang 
                AU  - Wang, Tao 
                AU  - Xing, Jinchun 
                TI  - MiR-223-3p promotes cell proliferation and metastasis by downregulating SLC4A4 in clear cell renal cell carcinoma
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101763
                DO  - 10.18632/aging.101763
                SP  - 615
                EP  - 633
                PY  - 
                AB  - MicroRNAs (miRNAs) are known to affect the occurrence and progression of cancer. We therefore evaluated the involvement of miR-223-3p in renal cell cancer. MiR-223-3p was highly expressed in clear cell renal cell cancer tissues. Clear cell renal cell cancer patients with higher miR-223-3p expression had higher tumor stages and grades and poorer prognoses. In renal cancer cells, overexpression of miR-223-3p enhanced cell proliferation and metastasis, while inhibition of miR-223-3p reduced the malignant capacity of the cells. MiR-223-3p was found to bind directly to solute carrier family 4, member 4 (SLC4A4) mRNA, thereby reducing SLC4A4 mRNA and protein expression. SLC4A4 overexpression restrained cell proliferation and metastasis by suppressing Kirsten rat sarcoma viral oncogene (KRAS) expression in renal cancer cells. SLC4A4 expression correlated negatively with miR-223-3p expression in patient samples. Given that miR-223-3p suppressed the SLC4A4/KRAS axis, miR-223-3p gene therapy could be an effective treatment for renal cancer.
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Efficacy of remote ischemic conditioning on improving WMHs and cognition in very elderly patients with intracranial atherosclerotic stenosis

Da Zhou, Jiayue Ding, Jingyuan Ya, Liqun Pan, Chaobo Bai, Jingwei Guan, Zhongao Wang, Kexin Jin, Qi Yang, Xunming Ji, Ran Meng,

https://doi.org/10.18632/aging.101764 pp 634—648

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Zhou D, Ding J, Ya J, Pan L, Bai C, Guan J, Wang Z, Jin K, Yang Q, Ji X, Meng R, . Efficacy of remote ischemic conditioning on improving WMHs and cognition in very elderly patients with intracranial atherosclerotic stenosis. . 11:634-648. https://doi.org/10.18632/aging.101764

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                TY  - JOUR
                AU  - Zhou, Da 
                AU  - Ding, Jiayue 
                AU  - Ya, Jingyuan 
                AU  - Pan, Liqun 
                AU  - Bai, Chaobo 
                AU  - Guan, Jingwei 
                AU  - Wang, Zhongao 
                AU  - Jin, Kexin 
                AU  - Yang, Qi 
                AU  - Ji, Xunming 
                AU  - Meng, Ran 
                TI  - Efficacy of remote ischemic conditioning on improving WMHs and cognition in very elderly patients with intracranial atherosclerotic stenosis
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101764
                DO  - 10.18632/aging.101764
                SP  - 634
                EP  - 648
                PY  - 
                AB  - Our previous study revealed that remote ischemic conditioning (RIC) reduced the incidence of stroke or TIA in octo- and nonagenarians with intracranial atherosclerotic stenosis (ICAS). Herein, we aimed to investigate whether RIC would influence the progression of white matter hyperintensities (WMHs) and cognitive impairment in the same group of patients. Fifty-eight patients with ICAS were randomly assigned in a 1:1 ratio to receive standard medical treatment with RIC (n=30) versus sham-RIC (n=28). The RIC protocol consisted of 5 cycles of alternating 5-min ischemia and 5-min reperfusion applied in the bilateral upper arms twice daily for 300 days. The efficacy outcomes included WMHs change on T2 FLAIR sequences, estimated by the Fazekas scale and Scheltens scale, cognitive change as assessed by the MMSE and MoCA, and some clinical symptoms within 300-day follow-up. Compared with the baseline, RIC treatment significantly reduced Fazekas and Scheltens scores at both 180-day (both p&lt;0.05) and 300-day (both p&lt;0.01) follow-ups, whereas no such reduction was observed in the control group. In the RIC group, Fazekas scores were significantly lower at 300-day follow-up (p&lt;0.001) while Scheltens scores were significantly lower at both 180-day and 300-day follow-ups (both p&lt;0.001), as compared with the control group. There were statistically significant between-group differences in the overall MMSE or MoCA scores, favoring RIC at 180-day and 300-day follow-ups (all p&lt;0.05). RIC may serve as a promising adjunctive to standard medical therapy for preventing the progression of WMHs and ameliorating cognitive impairment in very elderly patients with ICAS.
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A novel six-microRNA-based model to improve prognosis prediction of breast cancer

Jianguo Lai, Hongli Wang, Zihao Pan, Fengxi Su,

https://doi.org/10.18632/aging.101767 pp 649—662

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Lai J, Wang H, Pan Z, Su F, . A novel six-microRNA-based model to improve prognosis prediction of breast cancer. . 11:649-662. https://doi.org/10.18632/aging.101767

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                TY  - JOUR
                AU  - Lai, Jianguo 
                AU  - Wang, Hongli 
                AU  - Pan, Zihao 
                AU  - Su, Fengxi 
                TI  - A novel six-microRNA-based model to improve prognosis prediction of breast cancer
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101767
                DO  - 10.18632/aging.101767
                SP  - 649
                EP  - 662
                PY  - 
                AB  - Current tumor-node-metastasis (TNM) stage is unable to accurately predict the overall survival (OS) in breast cancer (BC) patients. This study aimed to construct a microRNA (miRNA)-based model to improve survival prediction of BC. We confirmed 99 differentially expressed miRNAs (DEMs) in 1044 BC samples compared to 102 adjacent normal breast tissues from The Cancer Genome Atlas (TCGA) database. Prognostic DEMs were used to establish a miRNA-based nomogram via Cox regression model. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes analyses (KEGG) were executed to analyze target genes of miRNAs. A six-miRNA signature was screened to effectively distinguish high-risk patients in the primary and validation cohort (all P&lt;0.001). Furthermore, we established a novel prognostic model incorporating the six-miRNA signature and clinical risk factors to predict 5-year OS of BC. Time-dependent receiver operating characteristic analysis suggested that the predictive accuracy of the six-miRNA-based nomogram was distinctly higher than that of TNM stage (0.758 vs 0.650, P&lt;0.001). GO and KEGG pathway analyses showed that the 39 target genes mainly enrichment in protein binding, cytoplasm and MAPK signaling pathway. Our six-miRNA-based model is a reliable prognostic tool for survival prediction and provides information for individualized treatment decisions in BC patients.
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Association between height and circulating CD34-positive cells taken into account for the influence of enhanced production among elderly Japanese men: a cross-sectional study

Yuji Shimizu, Hirotomo Yamanashi, Yuko Noguchi, Jun Koyamatsu, Mako Nagayoshi, Kairi Kiyoura, Shoichi Fukui, Mami Tamai, Shin-Ya Kawashiri, Kazuhiko Arima, Takahiro Maeda,

https://doi.org/10.18632/aging.101768 pp 663—672

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Shimizu Y, Yamanashi H, Noguchi Y, Koyamatsu J, Nagayoshi M, Kiyoura K, Fukui S, Tamai M, Kawashiri S, Arima K, Maeda T, . Association between height and circulating CD34-positive cells taken into account for the influence of enhanced production among elderly Japanese men: a cross-sectional study. . 11:663-672. https://doi.org/10.18632/aging.101768

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                TY  - JOUR
                AU  - Shimizu, Yuji 
                AU  - Yamanashi, Hirotomo 
                AU  - Noguchi, Yuko 
                AU  - Koyamatsu, Jun 
                AU  - Nagayoshi, Mako 
                AU  - Kiyoura, Kairi 
                AU  - Fukui, Shoichi 
                AU  - Tamai, Mami 
                AU  - Kawashiri, Shin-Ya 
                AU  - Arima, Kazuhiko 
                AU  - Maeda, Takahiro 
                TI  - Association between height and circulating CD34-positive cells taken into account for the influence of enhanced production among elderly Japanese men: a cross-sectional study
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101768
                DO  - 10.18632/aging.101768
                SP  - 663
                EP  - 672
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Shimizu, Yuji 
                AU  - Yamanashi, Hirotomo 
                AU  - Noguchi, Yuko 
                AU  - Koyamatsu, Jun 
                AU  - Nagayoshi, Mako 
                AU  - Kiyoura, Kairi 
                AU  - Fukui, Shoichi 
                AU  - Tamai, Mami 
                AU  - Kawashiri, Shin-Ya 
                AU  - Arima, Kazuhiko 
                AU  - Maeda, Takahiro 
                TI  - Association between height and circulating CD34-positive cells taken into account for the influence of enhanced production among elderly Japanese men: a cross-sectional study
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101768
                DO  - 10.18632/aging.101768
                SP  - 663
                EP  - 672
                PY  - 
                AB  - Recent studies have revealed an inverse association between height and cardiovascular disease and that endothelial progenitor cells (CD34-positive cells) contribute to vascular maintenance, which is associated with cardiovascular disease. However, evidence of the association between height and CD34-positive positive cells among elderly participants is limited. To assess this association, we conducted a cross-sectional study of 231 elderly Japanese men aged 65–69. Since enhanced production of circulating CD34-positive cells in response to endothelial injury might act have a strong confounding effect on the association between height and circulating CD34-positive cells, the median value for the levels of these cells (0.93 cells/μL) was used to stratify the participants. Multivariable linear regression analysis demonstrated that height was significantly positively associated with circulating CD34-positive cells for those participants with low levels of circulating CD34-positive cells (n=114) but not for those with higher levels (n=117), with a multi-adjusted standardized parameter estimate (β) of 0.27 (p=0.008) for low and 0.11 (0.275) for higher circulating CD34-positive cell levels. The positive association is limited to participants with relatively low circulating CD34-positive cell levels, whose productivity of these cells is not activated. Our findings indicate that height is an indicator of vascular maintenance capability in elderly Japanese men.
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IDH mutation-specific radiomic signature in lower-grade gliomas

Xing Liu, Yiming Li, Shaowu Li, Xing Fan, Zhiyan Sun, Zhengyi Yang, Kai Wang, Zhong Zhang, Tao Jiang, Yong Liu, Lei Wang, Yinyan Wang,

https://doi.org/10.18632/aging.101769 pp 673—696

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Liu X, Li Y, Li S, Fan X, Sun Z, Yang Z, Wang K, Zhang Z, Jiang T, Liu Y, Wang L, Wang Y, . IDH mutation-specific radiomic signature in lower-grade gliomas. . 11:673-696. https://doi.org/10.18632/aging.101769

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Provider: 
 TY - JOUR
 AU - Liu, Xing 
 AU - Li, Yiming 
 AU - Li, Shaowu 
 AU - Fan, Xing 
 AU - Sun, Zhiyan 
 AU - Yang, Zhengyi 
 AU - Wang, Kai 
 AU - Zhang, Zhong 
 AU - Jiang, Tao 
 AU - Liu, Yong 
 AU - Wang, Lei 
 AU - Wang, Yinyan 
 TI - IDH mutation-specific radiomic signature in lower-grade gliomas
 JO - 
 JA - 
 VL - 11
 IS - 2
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101769
 DO - 10.18632/aging.101769
 SP - 673
 EP - 696
 PY - 
 AB - Unravelling the heterogeneity is the central challenge for glioma precession oncology. In this study, we extracted quantitative image features from T2-weighted MR images and revealed that the isocitrate dehydrogenase (IDH) wild type and mutant lower grade gliomas (LGGs) differed in their expression of 146 radiomic descriptors. The logistic regression model algorithm further reduced these to 86 features. The classification model could discriminate the two types in both the training and validation sets with area under the curve values of 1.0000 and 0.9932, respectively. The transcriptome-radiomic analysis revealed that these features were associated with the immune response, biological adhesion, and several malignant behaviors, all of which are consistent with biological processes that are differentially expressed in IDH wild type and IDH mutant LGGs. Finally, a prognostic signature showed an ability to stratify IDH mutant LGGs into high and low risk groups with distinctive outcomes. By extracting a large number of radiomic features, we identified an IDH mutation-specific radiomic signature with prognostic implications. This radiomic signature may provide a way to non-invasively discriminate lower-grade gliomas as with or without the IDH mutation.
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Chronic hyperglycemia regulates microglia polarization through ERK5

Congde Chen, Suichun Wu, Zipu Hong, Xiaoming Chen, Xiaoou Shan, Shane Fischbach, Xiangwei Xiao,

https://doi.org/10.18632/aging.101770 pp 697—706

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Chen C, Wu S, Hong Z, Chen X, Shan X, Fischbach S, Xiao X, . Chronic hyperglycemia regulates microglia polarization through ERK5. . 11:697-706. https://doi.org/10.18632/aging.101770

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                TY  - JOUR
                AU  - Chen, Congde 
                AU  - Wu, Suichun 
                AU  - Hong, Zipu 
                AU  - Chen, Xiaoming 
                AU  - Shan, Xiaoou 
                AU  - Fischbach, Shane 
                AU  - Xiao, Xiangwei 
                TI  - Chronic hyperglycemia regulates microglia polarization through ERK5
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101770
                DO  - 10.18632/aging.101770
                SP  - 697
                EP  - 706
                PY  - 
                AB  - Diabetic patients are prone to developing Alzheimer’s disease (AD), in which microglia play a critical role. However, the direct effect of high glucose (HG) on microglia and the role of extracellular-signal-regulated kinase 5 (ERK5) signaling in this interaction have not been examined before. Here, these questions were addressed in microglia cultured in HG versus normal glucose (NG) conditions. Initially, HG induced microglial differentiation into the M2a phenotype with concomitant ERK5 activation. However, longer exposure to HG further induced differentiation of microglia into the M2b-like phenotype, followed by the M1-like subtype, concomitant with a gradual loss of ERK5 activation. BIX021895, a specific inhibitor of ERK5 activation, prevented M2a- differentiation of microglia, but induced earlier M2b-like polarization followed by M1-like polarization. Transfection of microglia with a sustained activated form of MEK5 (MEK5DD) prolonged the duration of the M2a phenotype, and prevented later differentiation into the M2b/M1 subtype. Conditioned media from the M2a-polarized microglia reduced neuronal cell apoptosis in hypoxic condition, while media from M2b-like or M1-like microglia enhanced apoptosis. Together, our data suggest that chronic hyperglycemia may induce a gradual alteration of microglia polarization into an increasingly proinflammatory subtype, which could be suppressed by sustained activation of ERK5 signaling.
                ER  -

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Age-related immune-modulating properties of seminal fluid that control the severity of asthma are gender specific

Yuichi Niikura, Takashi Ishii, Jurika Murakami, Tomoya Narita, Yoko Fujita, Hiroaki Negishi, Yuji Taketani, Naomi Yamashita,

https://doi.org/10.18632/aging.101773 pp 707—723

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Niikura Y, Ishii T, Murakami J, Narita T, Fujita Y, Negishi H, Taketani Y, Yamashita N, . Age-related immune-modulating properties of seminal fluid that control the severity of asthma are gender specific. . 11:707-723. https://doi.org/10.18632/aging.101773

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                TY  - JOUR
                AU  - Niikura, Yuichi 
                AU  - Ishii, Takashi 
                AU  - Murakami, Jurika 
                AU  - Narita, Tomoya 
                AU  - Fujita, Yoko 
                AU  - Negishi, Hiroaki 
                AU  - Taketani, Yuji 
                AU  - Yamashita, Naomi 
                TI  - Age-related immune-modulating properties of seminal fluid that control the severity of asthma are gender specific
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101773
                DO  - 10.18632/aging.101773
                SP  - 707
                EP  - 723
                PY  - 
                AB  - Reproductive organs play a pivotal role in asthma development and progression, especially in women. Endocrine environment changes associated with the menstrual cycle, pregnancy, and menopause can exacerbate the clinical features of asthma. Factors secreted by reproductive organs may be responsible for the gender difference and age-related changes in adult asthma. Here, we show that mammalian seminal fluid has anti-asthma effects exclusively in females. Exposure to murine seminal fluid markedly reduced eosinophilic airway inflammation in 2-month-old female mice upon ovalbumin inhalation. The anti-asthma effect with seminal fluid from 10-month-old males was double that with fluid from 2-month-old males, suggesting that it depended on male sexual maturation. We further found that seminal fluid from middle-aged human volunteers had beneficial effects in asthmatic female mice; these effects were associated with transcriptional repression of osteopontin and IL-17A, which are poor prognostic factors for asthma. In 2-month-old male mice, however, human seminal fluid failed to decrease asthmatic features and even enhanced osteopontin and IL-17A transcription. Our data demonstrate that age-related seminal fluid exerts opposing effects in asthmatic male and female mice. These findings may help the development of novel approaches to control the prevalence and age-related progression of asthma in women.
                ER  -

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CD56-negative NK cells with impaired effector function expand in CMV and EBV co-infected healthy donors with age

Bojana Müller-Durovic, Jasmin Grählert, Oliver P. Devine, Arne N. Akbar, Christoph Hess,

https://doi.org/10.18632/aging.101774 pp 724—740

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Müller-Durovic B, Grählert J, Devine OP, Akbar AN, Hess C, . CD56-negative NK cells with impaired effector function expand in CMV and EBV co-infected healthy donors with age. . 11:724-740. https://doi.org/10.18632/aging.101774

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                TY  - JOUR
                AU  - Müller-Durovic, Bojana 
                AU  - Grählert, Jasmin 
                AU  - Devine, Oliver P. 
                AU  - Akbar, Arne N. 
                AU  - Hess, Christoph 
                TI  - CD56-negative NK cells with impaired effector function expand in CMV and EBV co-infected healthy donors with age
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101774
                DO  - 10.18632/aging.101774
                SP  - 724
                EP  - 740
                PY  - 
                AB  - Natural killer cells lacking expression of CD56 (CD56neg NK cells) have been described in chronic HIV and hepatitis C virus infection. Features and functions of CD56neg NK cells in the context of latent infection with CMV and / or EBV with age are not known. In a cohort of healthy donors &gt;60 years of age, we found that co-infection with CMV and EBV drives expansion of CD56neg NK cells. Functionally, CD56neg NK cells displayed reduced cytotoxic capacity and IFN-γ production, a feature that was enhanced with CMV / EBV co-infection. Further, the frequency of CD56neg NK cells correlated with accumulation of end-stage-differentiated T cells and a reduced CD4 / CD8 T cell ratio, reflecting an immune risk profile. CD56neg NK cells had a mature phenotype characterized by low CD57 and KIR expression and lacked characteristics of cell senescence. No changes in their activating NK cell receptor expression, and no upregulation of the negative co-stimulation receptors PD-1 or TIM-3 were observed. In all, our data identify expansion of dysfunctional CD56neg NK cells in CMV+EBV+ elderly individuals suggesting that these cells may function as shape-shifters of cellular immunity and argue for a previously unrecognized role of EBV in mediating immune risk in the elderly.
                ER  -

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Association between antidiabetic agents use and leukocyte telomere shortening rates in patients with type 2 diabetes

Juanhong Liu, Yuanlong Ge, Shu Wu, Delin Ma, Weijie Xu, Ye Zhang, Yan Yang,

https://doi.org/10.18632/aging.101781 pp 741—755

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Liu J, Ge Y, Wu S, Ma D, Xu W, Zhang Y, Yang Y, . Association between antidiabetic agents use and leukocyte telomere shortening rates in patients with type 2 diabetes. . 11:741-755. https://doi.org/10.18632/aging.101781

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                TY  - JOUR
                AU  - Liu, Juanhong 
                AU  - Ge, Yuanlong 
                AU  - Wu, Shu 
                AU  - Ma, Delin 
                AU  - Xu, Weijie 
                AU  - Zhang, Ye 
                AU  - Yang, Yan 
                TI  - Association between antidiabetic agents use and leukocyte telomere shortening rates in patients with type 2 diabetes
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101781
                DO  - 10.18632/aging.101781
                SP  - 741
                EP  - 755
                PY  - 
                AB  - Telomere length and telomere shortening rate (TSR) are accepted indicators of aging in cross-sectional population studies. This study aimed to investigate the potential influence of common antidiabetic agents on telomere length and TSR in patients with type 2 diabetes mellitus (T2DM). Leukocyte telomere length was measured through terminal restriction fragment analysis, and TSR was calculated in 388 T2DM patients. Depending on whether or not they received antidiabetic medication, patients were first divided into a treatment group and a nontreatment group. Treated patients were further subdivided into an acarbose-free group (patients taking antidiabetic agents without acarbose) and an acarbose group (patients using acarbose for more than 3 months). Results showed that untreated patients had higher TSRs than patients on antidiabetic drugs. Interestingly, patients in the acarbose group had significantly higher TSRs than patients in the acarbose-free group. Compared to the nontreatment group, the acarbose group showed better glycemic control of HbA1c, but the TSR was also higher. Our results suggest that antidiabetic treatments without acarbose can slow aging. By contrast, acarbose may accelerate biological aging in patients with T2DM, independently of glycemic control.
                ER  -

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Lactobacillus paracasei PS23 decelerated age-related muscle loss by ensuring mitochondrial function in SAMP8 mice

Li-Han Chen, Shih-Yi Huang, Kuo-Chin Huang, Chih-Chieh Hsu, Kuen-Cheh Yang, Lin-Ai Li, Ching-Hung Chan, Hui-Yu Huang,

https://doi.org/10.18632/aging.101782 pp 756—770

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Chen L, Huang S, Huang K, Hsu C, Yang K, Li L, Chan C, Huang H, . Lactobacillus paracasei PS23 decelerated age-related muscle loss by ensuring mitochondrial function in SAMP8 mice. . 11:756-770. https://doi.org/10.18632/aging.101782

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Provider: 
 TY - JOUR
 AU - Chen, Li-Han 
 AU - Huang, Shih-Yi 
 AU - Huang, Kuo-Chin 
 AU - Hsu, Chih-Chieh 
 AU - Yang, Kuen-Cheh 
 AU - Li, Lin-Ai 
 AU - Chan, Ching-Hung 
 AU - Huang, Hui-Yu 
 TI - Lactobacillus paracasei PS23 decelerated age-related muscle loss by ensuring mitochondrial function in SAMP8 mice
 JO - 
 JA - 
 VL - 11
 IS - 2
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101782
 DO - 10.18632/aging.101782
 SP - 756
 EP - 770
 PY - 
 AB - Sarcopenia is a common impairment in the elderly population responsible for poor outcomes later in life; it can be caused by age-related alternations. Only a few strategies have been reported to reduce sarcopenia. Lactobacillus paracasei PS23 (LPPS23) has been reported to delay some age-related disorders. Therefore, here we investigated whether LPPS23 decelerates age-related muscle loss and its underlying mechanism. Female senescence-accelerated mouse prone-8 (SAMP8) mice were divided into three groups (n=6 each): non-aging (16-week-old), control (28-week-old), and PS23 (28-week-old) groups. The control and PS23 groups were given saline and LPPS23, respectively. We evaluated the effects of LPPS23 by analyzing body weight and composition, muscle strength, protein uptake, mitochondrial function, reactive oxygen species (ROS), antioxidant enzymes, and inflammation-related cytokines. LPPS23 significantly attenuated age-related decreases of muscle mass and strength. Compared to the control group, the non-aging and PS23 groups exhibited higher mitochondrial function, IL10, antioxidant enzymes, and protein uptake. Moreover, inflammatory cytokines and ROS were lower in the non-aging and PS23 groups than the control group. Taken together, LPPS23 extenuated sarcopenia progression during aging; this effect might have been enacted by preserving the mitochondrial function via reducing age-related inflammation and ROS and by retaining protein uptake in the SAMP8 mice.
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The curcumin analog EF24 is a novel senolytic agent

Wen Li, Yonghan He, Rongping Zhang, Guangrong Zheng, Daohong Zhou,

https://doi.org/10.18632/aging.101787 pp 771—782

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Li W, He Y, Zhang R, Zheng G, Zhou D, . The curcumin analog EF24 is a novel senolytic agent. . 11:771-782. https://doi.org/10.18632/aging.101787

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                TY  - JOUR
                AU  - Li, Wen 
                AU  - He, Yonghan 
                AU  - Zhang, Rongping 
                AU  - Zheng, Guangrong 
                AU  - Zhou, Daohong 
                TI  - The curcumin analog EF24 is a novel senolytic agent
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101787
                DO  - 10.18632/aging.101787
                SP  - 771
                EP  - 782
                PY  - 
                AB  - Cellular senescence is a hallmark of aging because senescent cells (SCs) accumulate with aging and play a causative role in age-related diseases. Selectively eliminating SCs has been emerging as a new strategy for treating age-related diseases and extending healthspan. Curcumin and its analogs have some anti-aging activities. However, the mechanisms of their action have not been fully elucidated. In the present study, we investigated whether various curcumin analogs can function as a senolytic agent. The results from our studies show that among these curcumin analogs EF24 is the most potent and broad-spectrum senolytic agent. Mechanistically, EF24 selectively kills SCs by inducing SC apoptosis in a reactive oxygen species (ROS) production independent manner but associated with an increase in the proteasome degradation of the Bcl-2 anti-apoptotic protein family proteins known to play an important role in protecting SCs from apoptosis. In addition, EF24 can synergistically kill SCs with ABT-263, a Bcl-2 and Bcl-xl inhibitor and a known senolytic agent. These findings provide new insights into the mechanisms by which curcumin analogs function as an anti-aging agent and suggest that the curcumin analog EF24 has the potential to be used as a novel senolytic agent for the treatment of age-related diseases.
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Superb book about Alzheimer’s disease

Iver Mysterud,

https://doi.org/10.18632/aging.101801 pp 783—786

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Mysterud I, . Superb book about Alzheimer’s disease. . 11:783-786. https://doi.org/10.18632/aging.101801

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                TY  - JOUR
                AU  - Mysterud, Iver 
                TI  - Superb book about Alzheimer’s disease
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101801
                DO  - 10.18632/aging.101801
                SP  - 783
                EP  - 786
                PY  - 
                AB  - The American physician and researcher Dale E. Bredesen's book The end of Alzheimer's from 2017 is probably the most important summary about this disease. It shows that there is justified hope of full recovery in early stages to Alzheimer's disease. For those who have already developed the disease, there is hope of significant improvement. The book is a well-written, popular scientific overview of the important approach Bredesen and his research group has worked with for the last few years. It should be read by all health conscious people, especially those who have passed 40 years, and professional neurologists and researchers will also benefit from it.
                ER  -

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Impact of Apolipoprotein E gene polymorphism during normal and pathological conditions of the brain across the lifespan

Diego Iacono, Gloria C. Feltis,

https://doi.org/10.18632/aging.101757 pp 787—816

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Iacono D, Feltis GC, . Impact of Apolipoprotein E gene polymorphism during normal and pathological conditions of the brain across the lifespan. . 11:787-816. https://doi.org/10.18632/aging.101757

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                TY  - JOUR
                AU  - Iacono, Diego 
                AU  - Feltis, Gloria C. 
                TI  - Impact of Apolipoprotein E gene polymorphism during normal and pathological conditions of the brain across the lifespan
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101757
                DO  - 10.18632/aging.101757
                SP  - 787
                EP  - 816
                PY  - 
                AB  - The central nervous system (CNS) is the cellular substrate for the integration of complex, dynamic, constant, and simultaneous interactions among endogenous and exogenous stimuli across the entire human lifespan. Numerous studies on aging-related brain diseases show that some genes identified as risk factors for some of the most common neurodegenerative diseases - such as the allele 4 of APOE gene (APOE4) for Alzheimer’s disease (AD) - have a much earlier neuro-anatomical and neuro-physiological impact. The impact of APOE polymorphism appears in fact to start as early as youth and early-adult life. Intriguingly, though, those same genes associated with aging-related brain diseases seem to influence different aspects of the brain functioning much earlier actually, that is, even from the neonatal periods and earlier. The APOE4, an allele classically associated with later-life neurodegenerative disorders as AD, seems in fact to exert a series of very early effects on phenomena of neuroplasticity and synaptogenesis that begin from the earliest periods of life such as the fetal ones.We reviewed some of the findings supporting the hypothesis that APOE polymorphism is an early modifier of various neurobiological aspects across the entire human lifespan - from the in-utero to the centenarian life - during both normal and pathological conditions of the brain.
                ER  -

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Can ovarian aging be delayed by pharmacological strategies?

Jinjin Zhang, Qian Chen, Dingfu Du, Tong Wu, Jingyi Wen, Meng Wu, Yan Zhang, Wei Yan, Su Zhou, Yan Li, Yan Jin, Aiyue Luo, Shixuan Wang,

https://doi.org/10.18632/aging.101784 pp 817—832

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Zhang J, Chen Q, Du D, Wu T, Wen J, Wu M, Zhang Y, Yan W, Zhou S, Li Y, Jin Y, Luo A, Wang S, . Can ovarian aging be delayed by pharmacological strategies?. . 11:817-832. https://doi.org/10.18632/aging.101784

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                TY  - JOUR
                AU  - Zhang, Jinjin 
                AU  - Chen, Qian 
                AU  - Du, Dingfu 
                AU  - Wu, Tong 
                AU  - Wen, Jingyi 
                AU  - Wu, Meng 
                AU  - Zhang, Yan 
                AU  - Yan, Wei 
                AU  - Zhou, Su 
                AU  - Li, Yan 
                AU  - Jin, Yan 
                AU  - Luo, Aiyue 
                AU  - Wang, Shixuan 
                TI  - Can ovarian aging be delayed by pharmacological strategies?
                JO  - 
                JA  - 
                VL  - 11
                IS  - 2
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101784
                DO  - 10.18632/aging.101784
                SP  - 817
                EP  - 832
                PY  - 
                AB  - Aging has been regarded as a treatable condition, and delaying aging could prevent some diseases. Ovarian aging, a special type of organ senescence, is the earliest-aging organ, as ovaries exhibit an accelerated rate of aging with characteristics of gradual declines in ovarian follicle quantity and quality since birth, compared to other organs. Ovarian aging is considered as the pacemaker of female body aging, which drives the aging of multiple organs of the body. Hence, anti-ovarian aging has become a research topic broadly interesting to both biomedical scientists and pharmaceutical industry. A marked progress has been made in exploration of possible anti-ovarian agents or approaches, such as calorie restriction mimetics, antioxidants, autophagy inducers etc., over the past years. This review is attempted to discuss recent advances in the area of anti-ovarian aging pharmacology and to offer new insights into our better understanding of molecular mechanisms underlying ovarian aging, which might be informative for future prevention and treatment of ovarian aging and its related diseases.
                ER  -

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The epigenetic clock: a molecular crystal ball for human aging?

Simone Ecker, Stephan Beck,

https://doi.org/10.18632/aging.101712 pp 833—835

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Correction: A functional variant of SMAD4 enhances macrophage recruitment and inflammatory response via TGF-β signal activation in Thoracic aortic aneurysm and dissection

Ying Wang, Pei Yin, Yi-Huan Chen, Yun-Sheng Yu, Wen-Xue Ye, Hao-Yue Huang, Zhen-Chun Ji, Zhen-Ya Shen,

https://doi.org/10.18632/aging.101812 pp 836

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Wang Y, Yin P, Chen Y, Yu Y, Ye W, Huang H, Ji Z, Shen Z, . Correction: A functional variant of SMAD4 enhances macrophage recruitment and inflammatory response via TGF-β signal activation in Thoracic aortic aneurysm and dissection. . 11:836-836. https://doi.org/10.18632/aging.101812

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Volume 11, Issue 2

About the Cover

Editorials

Ines Colmegna, Ursula Stochaj,

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Felice Gragnano, Negar Manavifar, Marco Valgimigli,

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Feilong Deng, Ying Li, Jiangchao Zhao,

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Barbara Garmy-Susini,

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Mudit Mishra, Ilayaraja Muthuramu, Bart De Geest,

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Edimar Alcides Bocchi, Mônica Samuel Avila, Silvia Moreira Ayub-Ferreira,

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Tracy Butler, Richard Bowen, Craig S. Atwood,

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Elizabeth Le Master, Irena Levitan,

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Diana Luz Juarez-Flores, Ingrid Gonzalez-Casacuberta, Gloria Garrabou,

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Research Papers

Ake T. Lu, Austin Quach, James G. Wilson, Alex P. Reiner, Abraham Aviv, Kenneth Raj, Lifang Hou, Andrea A. Baccarelli, Yun Li, James D. Stewart, Eric A. Whitsel, Themistocles L. Assimes, Luigi Ferrucci, Steve Horvath,

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Fengyan Jin, Xiangyu Zheng, Yanping Yang, Gang Yao, Long Ye, Thorsten R. Doeppner, Dirk M. Hermann, Haifeng Wang, Yun Dai,

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Jiafa He, Li Deng, Heping Liu, Taiying Chen, Shengying Chen, Shangzhou Xia, Yubin Liu,

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Lize Hermans, Celine Maes, Lisa Pauwels, Koen Cuypers, Kirstin-Friederike Heise, Stephan P. Swinnen, Inge Leunissen,

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Ravirajsinh N. Jadeja, Malita A. Jones, Ollya Fromal, Folami L. Powell, Sandeep Khurana, Nagendra Singh, Pamela M. Martin,

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Kazunori Sasaki, Julie Davies, Noelia Geribaldi Doldán, Sayo Arao, Farhana Ferdousi, Francis G. Szele, Hiroko Isoda,

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Yan Lin, Rong Liang, Yufen Qiu, Yufeng Lv, Jinyan Zhang, Gang Qin, Chunling Yuan, Zhihui Liu, Yongqiang Li, Donghua Zou, Yingwei Mao,

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Chenyang Duan, Zhezhe Cao, Fuqin Tang, Zhao Jian, Chunshui Liang, Hong Liu, Yingbin Xiao, Liangming Liu, Ruiyan Ma,

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Runchen Miao, Cuiyun Ge, Xing Zhang, Yang He, Xiaohua Ma, Xiaohong Xiang, Jingxian Gu, Yunong Fu, Kai Qu, Chang Liu, Qifei Wu, Ting Lin,

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Peng Lin, Yi-nan Guo, Lin Shi, Xiao-jiao Li, Hong Yang, Yun He, Qing Li, Yi-wu Dang, Kang-lai Wei, Gang Chen,

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