Volume 10, Issue 11

IDOL in metabolic, neurodegenerative and cardiovascular disease

Nienke M. van Loon, Patrick C.N. Rensen, Noam Zelcer,

https://doi.org/10.18632/aging.101597 pp 3042—3043

PDF How to Cite Request Reprint

Cite this Article

How to cite

van Loon NM, Rensen PC, Zelcer N, . IDOL in metabolic, neurodegenerative and cardiovascular disease. . 10:3042-3043. https://doi.org/10.18632/aging.101597

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Click to copy this citation from the text box above or download the citation:

MINOCA: current perspectives

Rocco A. Montone, Michele Russo, Giampaolo Niccoli,

https://doi.org/10.18632/aging.101618 pp 3044—3045

PDF How to Cite Request Reprint

Cardiovascular disease, inflammation, and mRNA stability

Allison B. Herman, Michael V. Autieri,

https://doi.org/10.18632/aging.101619 pp 3046—3047

PDF How to Cite Request Reprint

Implications of aging in the treatment of complex arrhythmias

Sofia Chatzidou, Georgios Georgiopoulos, Christos Kontogiannis,

https://doi.org/10.18632/aging.101620 pp 3048—3049

PDF How to Cite Request Reprint

Spatial navigation, aging and Alzheimer’s disease

Jan Laczó, Martina Parizkova, Scott D. Moffat,

https://doi.org/10.18632/aging.101634 pp 3050—3051

PDF How to Cite Request Reprint

Filamin A modulates platelet function

Jose J. Lopez, Isaac Jardin, Juan A. Rosado,

https://doi.org/10.18632/aging.101635 pp 3052—3053

PDF How to Cite Request Reprint

Do platelets LINE up for aging?

Hansjörg Schwertz, Matthew T. Rondina,

https://doi.org/10.18632/aging.101636 pp 3054—3055

PDF How to Cite Request Reprint

Blood pressure lowering in acute intracerebral hemorrhage

Olalla Pancorbo, David Rodriguez-Luna,

https://doi.org/10.18632/aging.101637 pp 3056—3057

PDF How to Cite Request Reprint

The heterogeneity within Alzheimer's disease

Daniel Ferreira, Lars-Olof Wahlund, Eric Westman,

https://doi.org/10.18632/aging.101638 pp 3058—3060

PDF How to Cite Request Reprint

Inflammatory markers and mediators in heart disease

Ana M. Valdes, Cristina Menni,

https://doi.org/10.18632/aging.101640 pp 3061—3062

PDF How to Cite Request Reprint

APP signaling in Alzheimer’s disease

Elena Anahi Bignante, Alfredo Lorenzo,

https://doi.org/10.18632/aging.101641 pp 3063—3064

PDF How to Cite Request Reprint

Aging clocks: disrupted circadian rhythms

Aiste Steponenaite, Stephany M. Biello, Gurprit S. Lall,

https://doi.org/10.18632/aging.101642 pp 3065—3066

PDF How to Cite Request Reprint

Disease or not, aging is easily treatable

Mikhail V. Blagosklonny,

https://doi.org/10.18632/aging.101647 pp 3067—3078

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Blagosklonny MV, . Disease or not, aging is easily treatable. . 10:3067-3078. https://doi.org/10.18632/aging.101647

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Blagosklonny, Mikhail V. 
                TI  - Disease or not, aging is easily treatable
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101647
                DO  - 10.18632/aging.101647
                SP  - 3067
                EP  - 3078
                PY  - 
                AB  - Is aging a disease? It does not matter because aging is already treated using a combination of several clinically-available drugs, including rapamycin. Whether aging is a disease depends on arbitrary definitions of both disease and aging. For treatment purposes, aging is a deadly disease (or more generally, pre-disease), despite being a normal continuation of normal organismal growth. It must and, importantly, can be successfully treated, thereby delaying classic age-related diseases such as cancer, cardiovascular and metabolic diseases, and neurodegeneration.
                ER  -

Click to copy this citation from the text box above or download the citation:

Aging and drug discovery

Daniela Bakula, Alexander M. Aliper, Polina Mamoshina, Michael A. Petr, Amanuel Teklu, Joseph A. Baur, Judith Campisi, Collin Y. Ewald, Anastasia Georgievskaya, Vadim N. Gladyshev, Olga Kovalchuk, Dudley W. Lamming, Martijn S. Luijsterburg, Alejandro Martín-Montalvo, Stuart Maudsley, Garik V. Mkrtchyan, Alexey Moskalev, S. Jay Olshansky, Ivan V. Ozerov, Alexander Pickett, Michael Ristow, Alex Zhavoronkov, Morten Scheibye-Knudsen,

https://doi.org/10.18632/aging.101646 pp 3079—3088

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Bakula D, Aliper AM, Mamoshina P, Petr MA, Teklu A, Baur JA, Campisi J, Ewald CY, Georgievskaya A, Gladyshev VN, Kovalchuk O, Lamming DW, Luijsterburg MS, et al, . Aging and drug discovery. . 10:3079-3088. https://doi.org/10.18632/aging.101646

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Bakula, Daniela 
                AU  - Aliper, Alexander M. 
                AU  - Mamoshina, Polina 
                AU  - Petr, Michael A. 
                AU  - Teklu, Amanuel 
                AU  - Baur, Joseph A. 
                AU  - Campisi, Judith 
                AU  - Ewald, Collin Y. 
                AU  - Georgievskaya, Anastasia 
                AU  - Gladyshev, Vadim N. 
                AU  - Kovalchuk, Olga 
                AU  - Lamming, Dudley W. 
                AU  - Luijsterburg, Martijn S. 
                AU  - Martín-Montalvo, Alejandro 
                AU  - Maudsley, Stuart 
                AU  - Mkrtchyan, Garik V. 
                AU  - Moskalev, Alexey 
                AU  - Olshansky, S. Jay 
                AU  - Ozerov, Ivan V. 
                AU  - Pickett, Alexander 
                AU  - Ristow, Michael 
                AU  - Zhavoronkov, Alex 
                AU  - Scheibye-Knudsen, Morten 
                TI  - Aging and drug discovery
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101646
                DO  - 10.18632/aging.101646
                SP  - 3079
                EP  - 3088
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Bakula, Daniela 
                AU  - Aliper, Alexander M. 
                AU  - Mamoshina, Polina 
                AU  - Petr, Michael A. 
                AU  - Teklu, Amanuel 
                AU  - Baur, Joseph A. 
                AU  - Campisi, Judith 
                AU  - Ewald, Collin Y. 
                AU  - Georgievskaya, Anastasia 
                AU  - Gladyshev, Vadim N. 
                AU  - Kovalchuk, Olga 
                AU  - Lamming, Dudley W. 
                AU  - Luijsterburg, Martijn S. 
                AU  - Martín-Montalvo, Alejandro 
                AU  - Maudsley, Stuart 
                AU  - Mkrtchyan, Garik V. 
                AU  - Moskalev, Alexey 
                AU  - Olshansky, S. Jay 
                AU  - Ozerov, Ivan V. 
                AU  - Pickett, Alexander 
                AU  - Ristow, Michael 
                AU  - Zhavoronkov, Alex 
                AU  - Scheibye-Knudsen, Morten 
                TI  - Aging and drug discovery
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101646
                DO  - 10.18632/aging.101646
                SP  - 3079
                EP  - 3088
                PY  - 
                AB  - Multiple interventions in the aging process have been discovered to extend the healthspan of model organisms. Both industry and academia are therefore exploring possible transformative molecules that target aging and age-associated diseases. In this overview, we summarize the presented talks and discussion points of the 5th Annual Aging and Drug Discovery Forum 2018 in Basel, Switzerland. Here academia and industry came together, to discuss the latest progress and issues in aging research. The meeting covered talks about the mechanistic cause of aging, how longevity signatures may be highly conserved, emerging biomarkers of aging, possible interventions in the aging process and the use of artificial intelligence for aging research and drug discovery. Importantly, a consensus is emerging both in industry and academia, that molecules able to intervene in the aging process may contain the potential to transform both societies and healthcare.
                ER  -

Click to copy this citation from the text box above or download the citation:

Glucose negatively affects Nrf2/SKN-1-mediated innate immunity in C. elegans

Le Li, Yi Chen, Changchi Chenzhao, Shuxiang Fu, Qumiao Xu, Jinfeng Zhao,

https://doi.org/10.18632/aging.101610 pp 3089—3103

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Li L, Chen Y, Chenzhao C, Fu S, Xu Q, Zhao J, . Glucose negatively affects Nrf2/SKN-1-mediated innate immunity in C. elegans. . 10:3089-3103. https://doi.org/10.18632/aging.101610

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Li, Le 
 AU - Chen, Yi 
 AU - Chenzhao, Changchi 
 AU - Fu, Shuxiang 
 AU - Xu, Qumiao 
 AU - Zhao, Jinfeng 
 TI - Glucose negatively affects Nrf2/SKN-1-mediated innate immunity in C. elegans
 JO - 
 JA - 
 VL - 10
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101610
 DO - 10.18632/aging.101610
 SP - 3089
 EP - 3103
 PY - 
 AB - High glucose levels negatively affect immune response. However, the underlying mechanisms are not well understood. Upon infection, the round worm C. elegans induces multiple gene transcription programs, including the Nrf2/SKN-1-mediated detoxification program, to activate the innate immunity. In this study, we find that high glucose conditions inhibit the SKN-1-mediated immune response to Salmonella typhimurium, exacerbate the infection and greatly decrease survival. The effect of glucose shows specificity to SKN-1 pathway, as UPRmit and UPRER that are known to be induced by infection, are not affected. Hyper-activation of SKN-1 by wdr-23 RNAi restores partly the immune response and increases the survival rate in response to S. typhimurium. In all, our study reveals a molecular pathway responsible for glucose’s negative effect on innate immunity, which could help to better understand diseases associated with hyperglycemia.
 ER -

Click to copy this citation from the text box above or download the citation:

Inactivation of glycogen synthase kinase-3α is required for mitochondria-mediated apoptotic germ cell phagocytosis in Sertoli cells

Yabin Gong, Zhilong Zhang, Zhanglin Chang, Hao Zhou, Ruqian Zhao, Bin He,

https://doi.org/10.18632/aging.101614 pp 3104—3116

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Gong Y, Zhang Z, Chang Z, Zhou H, Zhao R, He B, . Inactivation of glycogen synthase kinase-3α is required for mitochondria-mediated apoptotic germ cell phagocytosis in Sertoli cells. . 10:3104-3116. https://doi.org/10.18632/aging.101614

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Gong, Yabin 
                AU  - Zhang, Zhilong 
                AU  - Chang, Zhanglin 
                AU  - Zhou, Hao 
                AU  - Zhao, Ruqian 
                AU  - He, Bin 
                TI  - Inactivation of glycogen synthase kinase-3α is required for mitochondria-mediated apoptotic germ cell phagocytosis in Sertoli cells
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101614
                DO  - 10.18632/aging.101614
                SP  - 3104
                EP  - 3116
                PY  - 
                AB  - The rapid and efficient clearance of apoptotic germ cells (GCs) by Sertoli cells (SCs) is important for spermatogenesis. High mitochondrial activity in phagocytes is critical for continued clearance of apoptotic cells. However, the underlying molecular mechanism is poorly understood. Glycogen synthase kinase-3α (GSK3α) is a protein kinase that participates in the regulation of mitochondrial activity. Immunohistochemistry evidenced the predominant presence of the Ser21 phosphorylation GSK3α (inactivation) signal in SCs. Heat shock-induced apoptosis of GCs and dephosphorylation of GSK3α in SCs is a perfect model to investigate the role of GSK3α in phagocytic action. The number of apoptotic GCs was significantly lower in GSK3α inhibitor pre-treated mice with HS compared to normal control. In vitro phagocytosis assays shown that the phagocytic activity in GSK3α activated SCs was downregulated, while GSK3α inhibitor supplementation restored this process. Moreover, GSK3α activation participates in the alteration of the mitochondrial ultrastructure and activity. In particular, GSK3α activation inhibits mitochondrial fission via phosphorylation of dynamin related protein 1 at Ser637. Changes of mitochondrial activity resulted in the accumulation of lipid droplets and the alteration of metabolism pattern in SCs. In summary, our results demonstrate that inactivation of GSK3α is required for mitochondria-mediated apoptotic GCs phagocytosis in SCs.
                ER  -

Click to copy this citation from the text box above or download the citation:

Transferrin is responsible for mediating the effects of iron ions on the regulation of anterior pharynx-defective-1α/β and Presenilin 1 expression via PGE₂ and PGD₂ at the early stage of Alzheimer’s Disease

Chen-Di Lu, Ji-Kang Ma, Zheng-Yang Luo, Qun-Xi Tai, Pu Wang, Pei-Pei Guan,

https://doi.org/10.18632/aging.101615 pp 3117—3135

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Lu C, Ma J, Luo Z, Tai Q, Wang P, Guan P, . Transferrin is responsible for mediating the effects of iron ions on the regulation of anterior pharynx-defective-1α/β and Presenilin 1 expression via PGE₂ and PGD₂ at the early stage of Alzheimer’s Disease. . 10:3117-3135. https://doi.org/10.18632/aging.101615

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Lu, Chen-Di 
 AU - Ma, Ji-Kang 
 AU - Luo, Zheng-Yang 
 AU - Tai, Qun-Xi 
 AU - Wang, Pu 
 AU - Guan, Pei-Pei 
 TI - Transferrin is responsible for mediating the effects of iron ions on the regulation of anterior pharynx-defective-1α/β and Presenilin 1 expression via PGE2 and PGD2 at the early stage of Alzheimer’s Disease
 JO - 
 JA - 
 VL - 10
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101615
 DO - 10.18632/aging.101615
 SP - 3117
 EP - 3135
 PY - 
 AB - Transferrin (Tf) is an important iron-binding protein postulated to play a key role in iron ion (Fe) absorption via the Tf receptor (TfR), which potentially contributes to the pathogenesis of Alzheimer’s disease (AD). However, the role of Tf in AD remains unknown. Using mouse-derived neurons and APP/PS1 transgenic (Tg) mice as model systems, we firstly revealed the mechanisms of APH-1α/1β and presenilin 1 (PS1) upregulation by Fe in prostaglandin (PG) E2- and PGD2-dependent mechanisms. Specifically, Fe stimulated the expression of mPGES-1 and the production of PGE2 and PGD2 via the Tf and TfR system. Highly accumulated PGE2 markedly induced the expression of anterior pharynx-defective-1α and -1β (APH-1α/1β) and PS1 via an EP receptor-dependent mechanism. In contrast, PGD2 suppressed the expression of APH-1α/1β and PS1 via a prostaglandin D2 (DP) receptor-dependent mechanism. As the natural dehydrated product of PGD2, 15d-PGJ2 exerts inhibitory effects on the expression of APH-1α/1β and PS1 in a peroxisome proliferator-activated receptor (PPAR) γ-dependent manner. The expression of APH-1α/1β and PS1 ultimately determined the production and deposition of β-amyloid protein (Aβ), an effect that potentially contributes to the pathogenesis of AD.
 ER -

Click to copy this citation from the text box above or download the citation:

Egr-1 is involved in coronary microembolization-induced myocardial injury via Bim/Beclin-1 pathway-mediated autophagy inhibition and apoptosis activation

Xian-tao Wang, Xiao-dan Wu, Yuan-xi Lu, Yu-han Sun, Han-hua Zhu, Jia-bao Liang, Wen-kai He, Lang Li,

https://doi.org/10.18632/aging.101616 pp 3136—3147

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Wang X, Wu X, Lu Y, Sun Y, Zhu H, Liang J, He W, Li L, . Egr-1 is involved in coronary microembolization-induced myocardial injury via Bim/Beclin-1 pathway-mediated autophagy inhibition and apoptosis activation. . 10:3136-3147. https://doi.org/10.18632/aging.101616

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Wang, Xian-tao 
                AU  - Wu, Xiao-dan 
                AU  - Lu, Yuan-xi 
                AU  - Sun, Yu-han 
                AU  - Zhu, Han-hua 
                AU  - Liang, Jia-bao 
                AU  - He, Wen-kai 
                AU  - Li, Lang 
                TI  - Egr-1 is involved in coronary microembolization-induced myocardial injury via Bim/Beclin-1 pathway-mediated autophagy inhibition and apoptosis activation
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101616
                DO  - 10.18632/aging.101616
                SP  - 3136
                EP  - 3147
                PY  - 
                AB  - Coronary microembolization (CME) substantially reduces the clinical benefits of myocardial reperfusion therapy. Autophagy and apoptosis participate in the pathophysiological processes of almost all cardiovascular diseases, including CME-induced myocardial injury, but the precise underlying mechanisms remain unclear. In the present study, we observed that Egr-1 expression was substantially increased after CME modeling. Inhibition of Egr-1 expression through the targeted delivery of rAAV9-Egr-1-shRNA improved cardiac function and reduced myocardial injury. The microinfarct size was also significantly smaller in the Egr-1 inhibitor group than in the CME group. These benefits were partially reversed by the autophagy inhibitor 3-MA. As shown in our previous study, autophagy in the myocardium was impaired after CME. Inhibition of Egr-1 expression in vivo restored the autophagy flux and reduced myocardial apoptosis, at least partially, by inhibiting the Egr-1/Bim/Beclin-1 pathway, as evidenced by the results of the western blot, RT-qPCR, and TUNEL staining. At the same time, TEM showed a dramatic increase in the number of typical autophagic vacuoles in the Egr-1 inhibitor group compared to the CME group. Based on these findings, the Egr-1/Bim/Beclin-1 pathway may be involved in CME-induced myocardial injury by regulating myocardial autophagy and apoptosis, and this pathway represents a potential therapeutic target in CME.
                ER  -

Click to copy this citation from the text box above or download the citation:

BK channel overexpression on plasma membrane of fibroblasts from Hutchinson-Gilford progeria syndrome

Isabella Zironi, Entelë Gavoçi, Giovanna Lattanzi, Angela Virelli, Fabrizio Amorini, Daniel Remondini, Gastone Castellani,

https://doi.org/10.18632/aging.101621 pp 3148—3160

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zironi I, Gavoçi E, Lattanzi G, Virelli A, Amorini F, Remondini D, Castellani G, . BK channel overexpression on plasma membrane of fibroblasts from Hutchinson-Gilford progeria syndrome. . 10:3148-3160. https://doi.org/10.18632/aging.101621

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Zironi, Isabella 
                AU  - Gavoçi, Entelë 
                AU  - Lattanzi, Giovanna 
                AU  - Virelli, Angela 
                AU  - Amorini, Fabrizio 
                AU  - Remondini, Daniel 
                AU  - Castellani, Gastone 
                TI  - BK channel overexpression on plasma membrane of fibroblasts from Hutchinson-Gilford progeria syndrome
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101621
                DO  - 10.18632/aging.101621
                SP  - 3148
                EP  - 3160
                PY  - 
                AB  - Hutchinson-Gilford progeria syndrome (HGPS) is an extremely rare genetic disorder wherein symptoms resembling aspects of aging are manifested at a very early age. It is a genetic condition that occurs due to a de novo mutation in the LMNA gene encoding for the nuclear structural protein lamin A. The lamin family of proteins are thought to be involved in nuclear stability, chromatin structure and gene expression and this leads to heavy effects on the regulation and functionality of the cell machinery. The functional role of the large-conductance calcium-activated potassium channels (BKCa) is still unclear, but has been recently described a strong relationship with their membrane expression, progerin nuclear levels and the ageing process. In this study, we found that: i) the outward potassium membrane current amplitude and the fluorescence intensity of the BKCa channel probe showed higher values in human dermal fibroblast obtained from patients affected by HGPS if compared to that from healthy young subjects; ii) this result appears to correlate with a basic cellular activity such as the replicative boost. We suggest that studying the HGPS also from the electrophysiological point of view might reveal new clues about the normal process of aging.
                ER  -

Click to copy this citation from the text box above or download the citation:

AMPKα pathway involved in hepatic triglyceride metabolism disorder in diet-induced obesity mice following Escherichia coli Infection

Jing Fang, Fengyuan Wang, Hetao Song, Zhengyi Wang, Zhicai Zuo, Hengmin Cui, Yiping Jia, Junliang Deng, Shumin Yu, Yanchun Hu, Liuhong Shen, Xiaoping Ma, Zhihua Ren, Liping Gou,

https://doi.org/10.18632/aging.101623 pp 3161—3172

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Fang J, Wang F, Song H, Wang Z, Zuo Z, Cui H, Jia Y, Deng J, Yu S, Hu Y, Shen L, Ma X, Ren Z, et al, . AMPKα pathway involved in hepatic triglyceride metabolism disorder in diet-induced obesity mice following Escherichia coli Infection. . 10:3161-3172. https://doi.org/10.18632/aging.101623

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Fang, Jing 
 AU - Wang, Fengyuan 
 AU - Song, Hetao 
 AU - Wang, Zhengyi 
 AU - Zuo, Zhicai 
 AU - Cui, Hengmin 
 AU - Jia, Yiping 
 AU - Deng, Junliang 
 AU - Yu, Shumin 
 AU - Hu, Yanchun 
 AU - Shen, Liuhong 
 AU - Ma, Xiaoping 
 AU - Ren, Zhihua 
 AU - Gou, Liping 
 TI - AMPKα pathway involved in hepatic triglyceride metabolism disorder in diet-induced obesity mice following Escherichia coli Infection
 JO - 
 JA - 
 VL - 10
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101623
 DO - 10.18632/aging.101623
 SP - 3161
 EP - 3172
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Fang, Jing 
 AU - Wang, Fengyuan 
 AU - Song, Hetao 
 AU - Wang, Zhengyi 
 AU - Zuo, Zhicai 
 AU - Cui, Hengmin 
 AU - Jia, Yiping 
 AU - Deng, Junliang 
 AU - Yu, Shumin 
 AU - Hu, Yanchun 
 AU - Shen, Liuhong 
 AU - Ma, Xiaoping 
 AU - Ren, Zhihua 
 AU - Gou, Liping 
 TI - AMPKα pathway involved in hepatic triglyceride metabolism disorder in diet-induced obesity mice following Escherichia coli Infection
 JO - 
 JA - 
 VL - 10
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101623
 DO - 10.18632/aging.101623
 SP - 3161
 EP - 3172
 PY - 
 AB - To investigate the different effects of acute pulmonary infection induced by Escherichia coli (E. coli) on lipid metabolism between diet-induced obesity (DIO, fed with high-fat diet) mice and lean mice. A total of 180 ICR mice were selected to be challenged intranasally with phosphate-buffered saline or 109 CFUs/mL of E. coli, and the body character indexes, biochemical indexes and expressions of genes and proteins involved in lipid metabolism were examined pre- and post-infection. Results revealed that, before infection, DIO mice had significantly higher body weight, adipose and liver indexes, free fatty acid and triglyceride contents than lean mice. After infection, increased free fatty acid and triglyceride contents, increased expressions of resistin, SREBP-1c, ACC1, FAS and SCD-1, and declined PPARα, CPT-1α expressions and AMPKα phosphorylation were detected in the infected group, while the change rates were more serious in the lean mice than the DIO mice. The above-mentioned findings verified that, after being infected with E. coli, hepatic lipid metabolism disorder was aggravated by activating SREBP-1c related lipid synthesis pathway and inhibiting PPARα related fatty acid oxidation pathway. However, infection-induced lipid metabolic disorders was slighter in the DIO mice than the lean mice through AMPKα pathway.
 ER -

Click to copy this citation from the text box above or download the citation:

Effects of senescent secretory phenotype acquisition on human retinal pigment epithelial stem cells

Raffaella Lazzarini, Michele Nicolai, Vittorio Pirani, Cesare Mariotti, Roberto Di Primio,

https://doi.org/10.18632/aging.101624 pp 3173—3184

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Lazzarini R, Nicolai M, Pirani V, Mariotti C, Di Primio R, . Effects of senescent secretory phenotype acquisition on human retinal pigment epithelial stem cells. . 10:3173-3184. https://doi.org/10.18632/aging.101624

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Lazzarini, Raffaella 
                AU  - Nicolai, Michele 
                AU  - Pirani, Vittorio 
                AU  - Mariotti, Cesare 
                AU  - Di Primio, Roberto 
                TI  - Effects of senescent secretory phenotype acquisition on human retinal pigment epithelial stem cells
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101624
                DO  - 10.18632/aging.101624
                SP  - 3173
                EP  - 3184
                PY  - 
                AB  - Regenerative medicine approaches based on mesenchymal stem cells (MSCs) are being investigated to treat several aging-associated diseases, including age-related macular degeneration (AMD). Loss of retinal pigment epithelium (RPE) cells occurs early in AMD, and their transplant has the potential to slow disease progression.The human RPE contains a subpopulation of cells - adult RPE stem cells (RPESCs) – that are capable of self-renewal and of differentiating into RPE cells in vitro. However, age-related MSC changes involve loss of function and acquisition of a senescence-associated secretory phenotype (SASP), which can contribute to the maintenance of a chronic state of low-grade inflammation in tissues and organs.In a previous study we isolated, characterized, and differentiated RPESCs. Here, we induced replicative senescence in RPESCs and tested their acquisition of the senescence phenotype and the SASP as well as the differentiation ability of young and senescent RPESCs.Senescent RPESCs showed a significantly reduced proliferation ability, high senescence-associated β-galactosidase activity, and SASP acquisition. RPE-specific genes were downregulated and p21 and p53 protein expression was upregulated.These findings document the effects of senescence and SASP acquisition on RPESC differentiation ability and highlight the need for a greater understanding of their role in AMD pathogenesis.
                ER  -

Click to copy this citation from the text box above or download the citation:

Identification of an energy metabolism-related signature associated with clinical prognosis in diffuse glioma

Zhengui Zhou, Ruoyu Huang, Ruichao Chai, Xiaohong Zhou, Zhiping Hu, Wenbiao Wang, Baoguo Chen, Lintao Deng, Yuqing Liu, Fan Wu,

https://doi.org/10.18632/aging.101625 pp 3185—3209

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zhou Z, Huang R, Chai R, Zhou X, Hu Z, Wang W, Chen B, Deng L, Liu Y, Wu F, . Identification of an energy metabolism-related signature associated with clinical prognosis in diffuse glioma. . 10:3185-3209. https://doi.org/10.18632/aging.101625

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Zhou, Zhengui 
                AU  - Huang, Ruoyu 
                AU  - Chai, Ruichao 
                AU  - Zhou, Xiaohong 
                AU  - Hu, Zhiping 
                AU  - Wang, Wenbiao 
                AU  - Chen, Baoguo 
                AU  - Deng, Lintao 
                AU  - Liu, Yuqing 
                AU  - Wu, Fan 
                TI  - Identification of an energy metabolism-related signature associated with clinical prognosis in diffuse glioma
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101625
                DO  - 10.18632/aging.101625
                SP  - 3185
                EP  - 3209
                PY  - 
                AB  - Now, numerous exciting findings have been yielded in the field of energy metabolism within glioma cells. In addition to aerobic glycolysis, multiple catabolic pathways are employed for energy production. However, the prognostic significance of energy metabolism in glioma remains obscure. Here, we explored the relationship between energy metabolism gene profile and outcome of diffuse glioma patients using The Cancer Genome Altas (TCGA) and Chinese Glioma Genome Altas (CGGA) datasets. Based on the gene expression profile, consensus clustering identified two robust clusters of glioma patients with distinguished prognostic and molecular features. With the Cox proportional hazards model with elastic net penalty, an energy metabolism-related signature was built to evaluate patients’ prognosis. Kaplan-Meier analysis found that the acquired signature could differentiate the outcome of low and high-risk groups of patients in both cohorts. Moreover, the signature, significantly associated with the clinical and molecular features, could serve as an independent prognostic factor for glioma patients. Gene Ontology (GO) and Gene Set Enrichment Analysis (GSEA) showed that gene sets correlated with high-risk group were involved in immune and inflammatory response, with the low-risk group were mainly related to glutamate receptor signaling pathway. Our results provided new insight into energy metabolism role in diffuse glioma.
                ER  -

Click to copy this citation from the text box above or download the citation:

Accelerated DNA methylation age and the use of antihypertensive medication among older adults

Xu Gao, Elena Colicino, Jincheng Shen, Allan C. Just, Jamaji C. Nwanaji-Enwerem, Cuicui Wang, Brent Coull, Xihong Lin, Pantel Vokonas, Yinan Zheng, Lifang Hou, Joel Schwartz, Andrea A. Baccarelli,

https://doi.org/10.18632/aging.101626 pp 3210—3228

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Gao X, Colicino E, Shen J, Just AC, Nwanaji-Enwerem JC, Wang C, Coull B, Lin X, Vokonas P, Zheng Y, Hou L, Schwartz J, Baccarelli AA, . Accelerated DNA methylation age and the use of antihypertensive medication among older adults. . 10:3210-3228. https://doi.org/10.18632/aging.101626

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Gao, Xu 
                AU  - Colicino, Elena 
                AU  - Shen, Jincheng 
                AU  - Just, Allan C. 
                AU  - Nwanaji-Enwerem, Jamaji C. 
                AU  - Wang, Cuicui 
                AU  - Coull, Brent 
                AU  - Lin, Xihong 
                AU  - Vokonas, Pantel 
                AU  - Zheng, Yinan 
                AU  - Hou, Lifang 
                AU  - Schwartz, Joel 
                AU  - Baccarelli, Andrea A. 
                TI  - Accelerated DNA methylation age and the use of antihypertensive medication among older adults
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101626
                DO  - 10.18632/aging.101626
                SP  - 3210
                EP  - 3228
                PY  - 
                AB  - The discrepancy of DNA methylation age (DNAmAge) with chronological age (termed as age acceleration, AA) has been identified to be associated with many aging-related health outcomes including hypertension. Since taking antihypertensive medication (AHM) could prevent aging-related diseases caused by hypertension, we hypothesized that using AHM could also reduce the AA. We examined this hypothesis among 546 males aged 55–85 years by exploring the associations of AHM use with AA and its change rate (ΔAA) in two visits with a median follow-up of 3.86 years. Horvath DNAmAge was derived from DNA methylation profiles measured by Illumina HumanMethylation450 BeadChip and information on AHM use was collected by physician interview. A general decreasing pattern of AA was observed between the two visits. After the fully adjusting for potential covariates including hypertension, any AHM use showed a cross-sectional significant association with higher AA at each visit, as well as a longitudinal association with increased ΔAA between visits. Particularly, relative to participants who never took any AHM, individuals with continuous AHM use had a higher ΔAA of 0.6 year/chronological year. This finding underlines that DNAmAge and AA may not be able to capture the preventive effects of AHMs that reduce cardiovascular risks and mortality.
                ER  -

Click to copy this citation from the text box above or download the citation:

Methanolic extract of Tamarix Gallica attenuates hyperhomocysteinemia induced AD-like pathology and cognitive impairments in rats

Maibouge Tanko Mahamane Salissou, Yacoubou Abdoul Razak Mahaman, Feiqi Zhu, Fang Huang, Yuman Wang, Zhendong Xu, Dan Ke, Qun Wang, Rong Liu, Jian-Zhi Wang, Bin Zhang, Xiaochuan Wang,

https://doi.org/10.18632/aging.101627 pp 3229—3248

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Salissou MTM, Mahaman YAR, Zhu F, Huang F, Wang Y, Xu Z, Ke D, Wang Q, Liu R, Wang J, Zhang B, Wang X, . Methanolic extract of Tamarix Gallica attenuates hyperhomocysteinemia induced AD-like pathology and cognitive impairments in rats. . 10:3229-3248. https://doi.org/10.18632/aging.101627

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Salissou, Maibouge Tanko Mahamane 
 AU - Mahaman, Yacoubou Abdoul Razak 
 AU - Zhu, Feiqi 
 AU - Huang, Fang 
 AU - Wang, Yuman 
 AU - Xu, Zhendong 
 AU - Ke, Dan 
 AU - Wang, Qun 
 AU - Liu, Rong 
 AU - Wang, Jian-Zhi 
 AU - Zhang, Bin 
 AU - Wang, Xiaochuan 
 TI - Methanolic extract of Tamarix Gallica attenuates hyperhomocysteinemia induced AD-like pathology and cognitive impairments in rats
 JO - 
 JA - 
 VL - 10
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101627
 DO - 10.18632/aging.101627
 SP - 3229
 EP - 3248
 PY - 
 AB - Although few drugs are available today for the management of Alzheimer’s disease (AD) and many plants and their extracts are extensively employed in animals’ studies and AD patients, yet no drug or plant extract is able to reverse AD symptoms adequately. In the present study, Tamarix gallica (TG), a naturally occurring plant known for its strong antioxidative, anti-inflammatory and anti-amyloidogenic properties, was evaluated on homocysteine (Hcy) induced AD-like pathology and cognitive impairments in rats. We found that TG attenuated Hcy-induced oxidative stress and memory deficits. TG also improved neurodegeneration and neuroinflammation by upregulating synaptic proteins such as PSD95 and synapsin 1 and downregulating inflammatory markers including CD68 and GFAP with concomitant decrease in proinflammatory mediators interlukin-1β (IL1β) and tumor necrosis factor α (TNFα). TG attenuated tau hyperphosphorylation at multiple AD-related sites through decreasing some kinases and increasing phosphatase activities. Moreover, TG rescued amyloid-β (Aβ) pathology through downregulating BACE1. Our data for the first time provide evidence that TG attenuates Hcy-induced AD-like pathological changes and cognitive impairments, making TG a promising candidate for the treatment of AD-associated pathological changes.
 ER -

Click to copy this citation from the text box above or download the citation:

PhotoAgeClock: deep learning algorithms for development of non-invasive visual biomarkers of aging

Eugene Bobrov, Anastasia Georgievskaya, Konstantin Kiselev, Artem Sevastopolsky, Alex Zhavoronkov, Sergey Gurov, Konstantin Rudakov, Maria del Pilar Bonilla Tobar, Sören Jaspers, Sven Clemann,

https://doi.org/10.18632/aging.101629 pp 3249—3259

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Bobrov E, Georgievskaya A, Kiselev K, Sevastopolsky A, Zhavoronkov A, Gurov S, Rudakov K, del Pilar Bonilla Tobar M, Jaspers S, Clemann S, . PhotoAgeClock: deep learning algorithms for development of non-invasive visual biomarkers of aging. . 10:3249-3259. https://doi.org/10.18632/aging.101629

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Bobrov, Eugene 
                AU  - Georgievskaya, Anastasia 
                AU  - Kiselev, Konstantin 
                AU  - Sevastopolsky, Artem 
                AU  - Zhavoronkov, Alex 
                AU  - Gurov, Sergey 
                AU  - Rudakov, Konstantin 
                AU  - del Pilar Bonilla Tobar, Maria 
                AU  - Jaspers, Sören 
                AU  - Clemann, Sven 
                TI  - PhotoAgeClock: deep learning algorithms for development of non-invasive visual biomarkers of aging
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101629
                DO  - 10.18632/aging.101629
                SP  - 3249
                EP  - 3259
                PY  - 
                AB  - Aging biomarkers are the qualitative and quantitative indicators of the aging processes of the human body. Estimation of biological age is important for assessing the physiological state of an organism. The advent of machine learning lead to the development of the many age predictors commonly referred to as the “aging clocks” varying in biological relevance, ease of use, cost, actionability, interpretability, and applications. Here we present and investigate a novel non-invasive class of visual photographic biomarkers of aging. We developed a simple and accurate predictor of chronological age using just the anonymized images of eye corners called the PhotoAgeClock. Deep neural networks were trained on 8414 anonymized high-resolution images of eye corners labeled with the correct chronological age. For people within the age range of 20 to 80 in a specific population, the model was able to achieve a mean absolute error of 2.3 years and 95% Pearson and Spearman correlation.
                ER  -

Click to copy this citation from the text box above or download the citation:

Overexpression of CBS and CSE genes affects lifespan, stress resistance and locomotor activity in Drosophila melanogaster

Mikhail Shaposhnikov, Ekaterina Proshkina, Lyubov Koval, Nadezhda Zemskaya, Alex Zhavoronkov, Alexey Moskalev,

https://doi.org/10.18632/aging.101630 pp 3260—3272

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Shaposhnikov M, Proshkina E, Koval L, Zemskaya N, Zhavoronkov A, Moskalev A, . Overexpression of CBS and CSE genes affects lifespan, stress resistance and locomotor activity in Drosophila melanogaster. . 10:3260-3272. https://doi.org/10.18632/aging.101630

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Shaposhnikov, Mikhail 
 AU - Proshkina, Ekaterina 
 AU - Koval, Lyubov 
 AU - Zemskaya, Nadezhda 
 AU - Zhavoronkov, Alex 
 AU - Moskalev, Alexey 
 TI - Overexpression of CBS and CSE genes affects lifespan, stress resistance and locomotor activity in Drosophila melanogaster
 JO - 
 JA - 
 VL - 10
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101630
 DO - 10.18632/aging.101630
 SP - 3260
 EP - 3272
 PY - 
 AB - Recent experimental studies highlighted the role of hydrogen sulfide (H2S) in aging and longevity. The cystathionine ß-synthase (CBS) and cystathionine γ-lyase (CSE) are the key enzymes responsible for H2S production. Here we investigated the geroprotective effects of CSE and CBS overexpression in Drosophila. Overexpression of CSE did not affect a lifespan and decrease (mitochondrial form of CSE) or increase (cytoplasmic form of CSE) age dynamics of locomotor activity, while overexpression of CBS increase median (by 12.5%) and maximum (by 6.9%) lifespan and locomotor activity. Increasing of both CSE and CBS expression levels resulted in thermotolerance, but the resistance to combination of arid and food-free conditions decreased. The resistance to oxidative stress (paraquat) was not affected in flies with overexpression of CBS and cytoplasmic CSE, but decreased in flies overexpressing mitochondrial form of CSE. Thus, transgene overexpression of the CSE and CBS in Drosophila induce similar effects on stress-resistance and locomotor activity, however lifespan extending effect was revealed for CBS overexpression only.
 ER -

Click to copy this citation from the text box above or download the citation:

Spindle pole body component 25 regulates stemness of prostate cancer cells

Feilun Cui, Huaming Tang, Jian Tan, Jianpeng Hu,

https://doi.org/10.18632/aging.101631 pp 3273—3282

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Cui F, Tang H, Tan J, Hu J, . Spindle pole body component 25 regulates stemness of prostate cancer cells. . 10:3273-3282. https://doi.org/10.18632/aging.101631

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Cui, Feilun 
                AU  - Tang, Huaming 
                AU  - Tan, Jian 
                AU  - Hu, Jianpeng 
                TI  - Spindle pole body component 25 regulates stemness of prostate cancer cells
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101631
                DO  - 10.18632/aging.101631
                SP  - 3273
                EP  - 3282
                PY  - 
                AB  - Spindle pole body component 25 (SPC25) is a component of NDC80 complex that controls spindle assembly checkpoint in the microtubule-binding domain of kinetochores. We recently showed that SPC25 is required for prostate cancer (PrC) cell proliferation and cell cycle progression, and here we investigated whether SPC25 may be a Cancer stem cell (CSC) marker in PrC. We found that the levels of SPC25 were higher in PrC samples than paired normal prostate tissue. The overall survival of PrC patients with high SPC25 was poorer than those with low SPC25. PrC cell lines were transduced with two vectors carrying a luciferase reporter and a mCherry fluorescent reporter under a cytomegalovirus promoter and a nuclear green fluorescent protein reporter under the control of a SPC25 promoter, respectively, to allow differentiating SPC25+ from SPC25- PrC cells by flow cytometry. Compared to SPC25- cells, SPC25+ cells formed significantly more tumor spheres in culture, appeared to be more resistant towards docetaxel-induced cell apoptosis, and generated larger tumors with higher frequency after serial adoptive transplantation. Thus, our data suggest that SPC25 may be highly expressed in the CSC-like cells in PrC and could be a promising target for effective treatment of PrC.
                ER  -

Click to copy this citation from the text box above or download the citation:

Uncoupling protein 4 (UCP4) gene variability in neurodegenerative disorders: further evidence of association in Frontotemporal dementia

Alberto Montesanto, Paolina Crocco, Serena Dato, Silvana Geracitano, Francesca Frangipane, Rosanna Colao, Raffaele Maletta, Giuseppe Passarino, Amalia C. Bruni, Giuseppina Rose,

https://doi.org/10.18632/aging.101632 pp 3283—3293

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Montesanto A, Crocco P, Dato S, Geracitano S, Frangipane F, Colao R, Maletta R, Passarino G, Bruni AC, Rose G, . Uncoupling protein 4 (UCP4) gene variability in neurodegenerative disorders: further evidence of association in Frontotemporal dementia. . 10:3283-3293. https://doi.org/10.18632/aging.101632

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Montesanto, Alberto 
 AU - Crocco, Paolina 
 AU - Dato, Serena 
 AU - Geracitano, Silvana 
 AU - Frangipane, Francesca 
 AU - Colao, Rosanna 
 AU - Maletta, Raffaele 
 AU - Passarino, Giuseppe 
 AU - Bruni, Amalia C. 
 AU - Rose, Giuseppina 
 TI - Uncoupling protein 4 (UCP4) gene variability in neurodegenerative disorders: further evidence of association in Frontotemporal dementia
 JO - 
 JA - 
 VL - 10
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101632
 DO - 10.18632/aging.101632
 SP - 3283
 EP - 3293
 PY - 
 AB - Ongoing research suggests that mitochondrial dysfunction is a common hallmark in neurodegenerative diseases, pointing to mitochondrial uncoupling process as a critical player. We recently reported that rs9472817-C/G, an intronic variant of neuronal mitochondrial uncoupling protein-4 (UCP4/SLC25A27) gene affects the risk of late onset Alzheimer's disease (LOAD), and that the variant's effect is strongly dependent on APOE-ε4 status. Here, we extended our analysis to a cohort of 751 subjects including late-onset familial and sporadic cases of frontotemporal dementia (FTD; 213), Parkinson disease (PD;96), and 442 healthy controls. In all subgroups, carriers of APOE-ε4 allele were at higher risk of disease. Regarding the rs9472817, no association was detected in familial FTD and both subgroups of PD patients. In sporadic FTD, as in LOAD, we found that the C allele increased the risk of disease of about 1.51-fold in a dose-dependent manner (p=0.013) independently from that conferred by APOE-ε4. Expression quantitative trait loci (eQTL) data of different brain regions suggest that rs9472817 likely exerts its effect by a cis-regulatory mechanism involving modulation of UCP4. If validated, the involvement of UCP4 in both FTD and LOAD might indicate interesting shared etiological factors which might give future therapeutic clues.
 ER -

Click to copy this citation from the text box above or download the citation:

Azithromycin and Roxithromycin define a new family of “senolytic” drugs that target senescent human fibroblasts

Bela Ozsvari, John R. Nuttall, Federica Sotgia, Michael P. Lisanti,

https://doi.org/10.18632/aging.101633 pp 3294—3307

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Ozsvari B, Nuttall JR, Sotgia F, Lisanti MP, . Azithromycin and Roxithromycin define a new family of “senolytic” drugs that target senescent human fibroblasts. . 10:3294-3307. https://doi.org/10.18632/aging.101633

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Ozsvari, Bela 
                AU  - Nuttall, John R. 
                AU  - Sotgia, Federica 
                AU  - Lisanti, Michael P. 
                TI  - Azithromycin and Roxithromycin define a new family of “senolytic” drugs that target senescent human fibroblasts
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101633
                DO  - 10.18632/aging.101633
                SP  - 3294
                EP  - 3307
                PY  - 
                AB  - Here, we employed a “senolytic” assay system as a screening tool, with the goal of identifying and repurposing FDA-approved antibiotics, for the targeting of the senescent cell population. Briefly, we used two established human fibroblast cell lines (MRC-5 and/or BJ) as model systems to induce senescence, via chronic treatment with a DNA-damaging agent, namely BrdU (at a concentration of 100 μM for 8 days). Cell viability was then monitored by using the SRB assay, to measure protein content. As a consequence of this streamlined screening strategy, we identified Azithromycin and Roxithromycin as two novel clinically-approved senolytic drugs. However, Erythromycin – the very closely-related parent compound – did not show any senolytic activity, highlighting the dramatic specificity of these interactions. Interestingly, we also show that Azithromycin treatment of human fibroblasts was indeed sufficient to strongly induce both aerobic glycolysis and autophagy. However, the effects of Azithromycin on mitochondrial oxygen consumption rates (OCR) were bi-phasic, showing inhibitory activity at 50 μM and stimulatory activity at 100 μM. These autophagic/metabolic changes induced by Azithromycin could mechanistically explain its senolytic activity. We also independently validated our findings using the xCELLigence real-time assay system, which measures electrical impedance. Using this approach, we see that Azithromycin preferentially targets senescent cells, removing approximately 97% of them with great efficiency. This represents a near 25-fold reduction in senescent cells. Finally, we also discuss our current results in the context of previous clinical findings that specifically document the anti-inflammatory activity of Azithromycin in patients with cystic fibrosis – a genetic lung disorder that results in protein mis-folding mutations that cause protein aggregation.
                ER  -

Click to copy this citation from the text box above or download the citation:

ZNF185 is a p53 target gene following DNA damage

Artem Smirnov, Angela Cappello, Anna Maria Lena, Lucia Anemona, Alessandro Mauriello, Nicola Di Daniele, Margherita Annicchiarico-Petruzzelli, Gerry Melino, Eleonora Candi,

https://doi.org/10.18632/aging.101639 pp 3308—3326

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Smirnov A, Cappello A, Lena AM, Anemona L, Mauriello A, Di Daniele N, Annicchiarico-Petruzzelli M, Melino G, Candi E, . ZNF185 is a p53 target gene following DNA damage. . 10:3308-3326. https://doi.org/10.18632/aging.101639

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Smirnov, Artem 
                AU  - Cappello, Angela 
                AU  - Lena, Anna Maria 
                AU  - Anemona, Lucia 
                AU  - Mauriello, Alessandro 
                AU  - Di Daniele, Nicola 
                AU  - Annicchiarico-Petruzzelli, Margherita 
                AU  - Melino, Gerry 
                AU  - Candi, Eleonora 
                TI  - ZNF185 is a p53 target gene following DNA damage
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101639
                DO  - 10.18632/aging.101639
                SP  - 3308
                EP  - 3326
                PY  - 
                AB  - The transcription factor p53 is a key player in the tumour suppressive DNA damage response and a growing number of target genes involved in these pathways has been identified. p53 has been shown to be implicated in controlling cell motility and its mutant form enhances metastasis by loss of cell directionality, but the p53 role in this context has not yet being investigated. Here, we report that ZNF185, an actin cytoskeleton-associated protein from LIM-family of Zn-finger proteins, is induced following DNA-damage. ChIP-seq analysis, chromatin crosslinking immune-precipitation experiments and luciferase assays demonstrate that ZNF185 is a bona fide p53 target gene. Upon genotoxic stress, caused by DNA-damaging drug etoposide and UVB irradiation, ZNF185 expression is up-regulated and in etoposide-treated cells, ZNF185 depletion does not affect cell proliferation and apoptosis, but interferes with actin cytoskeleton remodelling and cell polarization. Bioinformatic analysis of different types of epithelial cancers from both TCGA and GTEx databases showed a significant decrease in ZNF185 mRNA level compared to normal tissues. These findings are confirmed by tissue micro-array IHC staining. Our data highlight the involvement of ZNF185 and cytoskeleton changes in p53-mediated cellular response to genotoxic stress and indicate ZNF185 as potential biomarker for epithelial cancer diagnosis.
                ER  -

Click to copy this citation from the text box above or download the citation:

Oxidative muscles have better mitochondrial homeostasis than glycolytic muscles throughout life and maintain mitochondrial function during aging

Annunziata N. Crupi, Jordan S. Nunnelee, David J. Taylor, Amandine Thomas, Jean-Philippe Vit, Celine E. Riera, Roberta A. Gottlieb, Helen S. Goodridge,

https://doi.org/10.18632/aging.101643 pp 3327—3352

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Crupi AN, Nunnelee JS, Taylor DJ, Thomas A, Vit J, Riera CE, Gottlieb RA, Goodridge HS, . Oxidative muscles have better mitochondrial homeostasis than glycolytic muscles throughout life and maintain mitochondrial function during aging. . 10:3327-3352. https://doi.org/10.18632/aging.101643

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Crupi, Annunziata N. 
                AU  - Nunnelee, Jordan S. 
                AU  - Taylor, David J. 
                AU  - Thomas, Amandine 
                AU  - Vit, Jean-Philippe 
                AU  - Riera, Celine E. 
                AU  - Gottlieb, Roberta A. 
                AU  - Goodridge, Helen S. 
                TI  - Oxidative muscles have better mitochondrial homeostasis than glycolytic muscles throughout life and maintain mitochondrial function during aging
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101643
                DO  - 10.18632/aging.101643
                SP  - 3327
                EP  - 3352
                PY  - 
                AB  - Preservation of mitochondrial function, which is dependent on mitochondrial homeostasis (biogenesis, dynamics, disposal/recycling), is critical for maintenance of skeletal muscle function. Skeletal muscle performance declines upon aging (sarcopenia) and is accompanied by decreased mitochondrial function in fast-glycolytic muscles. Oxidative metabolism promotes mitochondrial homeostasis, so we investigated whether mitochondrial function is preserved in oxidative muscles. We compared tibialis anterior (predominantly glycolytic) and soleus (oxidative) muscles from young (3 mo) and old (28-29 mo) C57BL/6J mice. Throughout life, the soleus remained more oxidative than the tibialis anterior and expressed higher levels of markers of mitochondrial biogenesis, fission/fusion and autophagy. The respiratory capacity of mitochondria isolated from the tibialis anterior, but not the soleus, declined upon aging. The soleus and tibialis anterior exhibited similar aging-associated changes in mitochondrial biogenesis, fission/fusion, disposal and autophagy marker expression, but opposite changes in fiber composition: the most oxidative fibers declined in the tibialis anterior, while the more glycolytic fibers declined in the soleus. In conclusion, oxidative muscles are protected from mitochondrial aging, probably due to better mitochondrial homeostasis ab initio and aging-associated changes in fiber composition. Exercise training aimed at enriching oxidative fibers may be valuable in preventing mitochondria-related aging and its contribution to sarcopenia.
                ER  -

Click to copy this citation from the text box above or download the citation:

LOC134466 methylation promotes oncogenesis of endometrial carcinoma through LOC134466/hsa-miR-196a-5p/TAC1 axis

Hai Xu, Yuan Sun, Zhen Ma, Xin Xu, Lili Qin, Baoping Luo,

https://doi.org/10.18632/aging.101644 pp 3353—3370

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Xu H, Sun Y, Ma Z, Xu X, Qin L, Luo B, . LOC134466 methylation promotes oncogenesis of endometrial carcinoma through LOC134466/hsa-miR-196a-5p/TAC1 axis. . 10:3353-3370. https://doi.org/10.18632/aging.101644

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Xu, Hai 
 AU - Sun, Yuan 
 AU - Ma, Zhen 
 AU - Xu, Xin 
 AU - Qin, Lili 
 AU - Luo, Baoping 
 TI - LOC134466 methylation promotes oncogenesis of endometrial carcinoma through LOC134466/hsa-miR-196a-5p/TAC1 axis
 JO - 
 JA - 
 VL - 10
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101644
 DO - 10.18632/aging.101644
 SP - 3353
 EP - 3370
 PY - 
 AB - To investigate possible mechanism of abnormal methylation of long non-coding RNA (lncRNA) on endometrial carcinoma (EC) progression, we detected the genome methylation profiling of endometrial carcinoma by bioinformatic analysis. Accordingly, gene LOC134466 was chosen for the further research. We also found that TAC1 was the target gene of LOC134466 and miRNA, hsa-miR-196a-5p, might form a connection between LOC134466 and TAC1. The relationship was further proved by dual-luciferase reporter assay. In vitro studies, DNA methylation and expression were determined by MSP and qRT-PCR respectively. Cell proliferation, apoptosis and cell cycle were demonstrated by colony formation assay, Annexin V/PI double staining and flow cytometry. Besides, the function of LOC134466 and TAC1 in EC was further confirmed by Tumor Xenograft. Our results indicated that EC progression was promoted by hypermethylated LOC134466 and TAC1. Moreover, TAC1 transcription was regulated by LOC134466 via hsa-miR-196a-5p binding. LOC134466 and TAC1 demethylation by 5-Aza-2-Deoxycytidine inhibited EC cells proliferation and accelerated cell apoptosis. Furthermore, the expression of TACR1, TACR2 and TACR3 was remarkably decreased through LOC134466 and TAC1 treatments. Our findings establish a novel regulatory axis, LOC134466/hsa-miR-196a-5p/TAC1. Downregulation of the axis promoted EC development through TACR3, which further activated neuroactive ligand-receptor interaction.
 ER -

Click to copy this citation from the text box above or download the citation:

LncRNA CDKN2BAS predicts poor prognosis in patients with hepatocellular carcinoma and promotes metastasis via the miR-153-5p/ARHGAP18 signaling axis

Junzheng Chen, Xitian Huang, Weijun Wang, Hongcheng Xie, Jianfeng Li, Zhenfen Hu, Zhijian Zheng, Huiyong Li, Lingfang Teng,

https://doi.org/10.18632/aging.101645 pp 3371—3381

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Chen J, Huang X, Wang W, Xie H, Li J, Hu Z, Zheng Z, Li H, Teng L, . LncRNA CDKN2BAS predicts poor prognosis in patients with hepatocellular carcinoma and promotes metastasis via the miR-153-5p/ARHGAP18 signaling axis. . 10:3371-3381. https://doi.org/10.18632/aging.101645

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Chen, Junzheng 
                AU  - Huang, Xitian 
                AU  - Wang, Weijun 
                AU  - Xie, Hongcheng 
                AU  - Li, Jianfeng 
                AU  - Hu, Zhenfen 
                AU  - Zheng, Zhijian 
                AU  - Li, Huiyong 
                AU  - Teng, Lingfang 
                TI  - LncRNA CDKN2BAS predicts poor prognosis in patients with hepatocellular carcinoma and promotes metastasis via the miR-153-5p/ARHGAP18 signaling axis
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101645
                DO  - 10.18632/aging.101645
                SP  - 3371
                EP  - 3381
                PY  - 
                AB  - Background: Growing evidence shows that long noncoding RNAs (lncRNAs) play a crucial role in cancer progression. However, whether lncRNA CDKN2BAS is involved in human hepatocellular carcinoma (HCC) metastasis remains unclear.Methods: Human lncRNA microarray analysis was performed to detect differential expression levels of lncRNAs in metastatic HCC tissues. Effects of CDKN2BAS on cell proliferation, migration, and apoptosis were determined by MTT assay, colony formation assay, migration assay, scratch assay, and flow cytometry. The xenograft experiment was used to confirm the effect of CDKN2BAS on HCC in vivo. qRT-PCR and Western blot were performed to determine the expression levels of mRNAs and proteins. Luciferase reporter assay was used to identify the specific target relationships.Results: CDKN2BAS was remarkably up-regulated in metastatic HCC tissues compared with the adjacent non-tumor tissues. CDKN2BAS promotes HCC cell growth and migration in vitro and in vivo. Additionally, CDKN2BAS upregulated the expression of Rho GTPase activating protein 18 (ARHGAP18) by sponging microRNA-153-5p (miR-153-5p), and thus promoted HCC cell migration. Besides, CDKN2BAS downregulated the expression of Krüppel-like factor 13 (KLF13) and activated MEK-ERK1/2 signaling, thus reducing apoptosis in HCC cells.Conclusions: Our study revealed that lncRNA CDKN2BAS promotes HCC metastasis by regulating the miR-153-5p/ARHGAP18 signaling.
                ER  -

Click to copy this citation from the text box above or download the citation:

Greater loss of mitochondrial function with ageing is associated with earlier onset of sarcopenia in C. elegans

Christopher J. Gaffney, Amelia Pollard, Thomas F. Barratt, Dumitru Constantin-Teodosiu, Paul L. Greenhaff, Nathaniel J. Szewczyk,

https://doi.org/10.18632/aging.101654 pp 3382—3396

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Gaffney CJ, Pollard A, Barratt TF, Constantin-Teodosiu D, Greenhaff PL, Szewczyk NJ, . Greater loss of mitochondrial function with ageing is associated with earlier onset of sarcopenia in C. elegans. . 10:3382-3396. https://doi.org/10.18632/aging.101654

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Gaffney, Christopher J. 
 AU - Pollard, Amelia 
 AU - Barratt, Thomas F. 
 AU - Constantin-Teodosiu, Dumitru 
 AU - Greenhaff, Paul L. 
 AU - Szewczyk, Nathaniel J. 
 TI - Greater loss of mitochondrial function with ageing is associated with earlier onset of sarcopenia in C. elegans
 JO - 
 JA - 
 VL - 10
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101654
 DO - 10.18632/aging.101654
 SP - 3382
 EP - 3396
 PY - 
 AB - Sarcopenia, the age-related decline of muscle, is a significant and growing public health burden. C. elegans, a model organism for investigating the mechanisms of ageing, also displays sarcopenia, but the underlying mechanism(s) remain elusive. Here, we use C. elegans natural scaling of lifespan in response to temperature to examine the relationship between mitochondrial content, mitochondrial function, and sarcopenia. Mitochondrial content and maximal mitochondrial ATP production rates (MAPR) display an inverse relationship to lifespan, while onset of MAPR decline displays a direct relationship. Muscle mitochondrial structure, sarcomere structure, and movement decline also display a direct relationship with longevity. Notably, the decline in mitochondrial network structure occurs earlier than sarcomere decline, and correlates more strongly with loss of movement, and scales with lifespan. These results suggest that mitochondrial function is critical in the ageing process and more robustly explains the onset and progression of sarcopenia than loss of sarcomere structure.
 ER -

Click to copy this citation from the text box above or download the citation:

Cell cycle-dependent and -independent telomere shortening accompanies murine brain aging

Quratul Ain, Christian Schmeer, Diane Penndorf, Mike Fischer, Tzvetanka Bondeva, Martin Förster, Ronny Haenold, Otto W Witte, Alexandra Kretz,

https://doi.org/10.18632/aging.101655 pp 3397—3420

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Ain Q, Schmeer C, Penndorf D, Fischer M, Bondeva T, Förster M, Haenold R, Witte OW, Kretz A, . Cell cycle-dependent and -independent telomere shortening accompanies murine brain aging. . 10:3397-3420. https://doi.org/10.18632/aging.101655

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Ain, Quratul 
                AU  - Schmeer, Christian 
                AU  - Penndorf, Diane 
                AU  - Fischer, Mike 
                AU  - Bondeva, Tzvetanka 
                AU  - Förster, Martin 
                AU  - Haenold, Ronny 
                AU  - Witte, Otto W 
                AU  - Kretz, Alexandra 
                TI  - Cell cycle-dependent and -independent telomere shortening accompanies murine brain aging
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101655
                DO  - 10.18632/aging.101655
                SP  - 3397
                EP  - 3420
                PY  - 
                AB  - Replication-based telomere shortening during lifetime is species- and tissue-specific, however, its impact on healthy aging is unclear. In particular, the contribution of telomere truncation to the aging process of the CNS, where replicative senescence alone fails to explain organ aging due to low to absent mitotic activity of intrinsic populations, is undefined. Here, we assessed changes in relative telomere length in non-replicative and replicative neural brain populations and telomerase activity as a function of aging in C57BL/6 mice. Telomeres in neural cells and sub-selected neurons shortened with aging in a cell cycle-dependent and -independent manner, with preponderance in replicative moieties, implying that proliferation accelerates, but is not prerequisite for telomere shortening. Consistent with this telomere erosion, telomerase activity and nuclear TERT protein were not induced with aging. Knockdown of the Rela subunit of NF-κB, which controls both telomerase enzyme and subcellular TERT protein allocation, did also not influence telomerase activity or telomere length, in spite of its naive up-regulation selectively under aging conditions. We conclude that telomere instability is intrinsic to physiological brain aging beyond cell replication, and appears to occur independently of a functional interplay with NF-κB, but rather as a failure to induce or relocate telomerase.
                ER  -

Click to copy this citation from the text box above or download the citation:

miR-150-5p suppresses tumor progression by targeting VEGFA in colorectal cancer

Xiaoxiang Chen, Xueni Xu, Bei Pan, Kaixuan Zeng, Mu Xu, Xiangxiang Liu, Bangshun He, Yuqin Pan, Huiling Sun, Shukui Wang,

https://doi.org/10.18632/aging.101656 pp 3421—3437

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Chen X, Xu X, Pan B, Zeng K, Xu M, Liu X, He B, Pan Y, Sun H, Wang S, . miR-150-5p suppresses tumor progression by targeting VEGFA in colorectal cancer. . 10:3421-3437. https://doi.org/10.18632/aging.101656

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Chen, Xiaoxiang 
                AU  - Xu, Xueni 
                AU  - Pan, Bei 
                AU  - Zeng, Kaixuan 
                AU  - Xu, Mu 
                AU  - Liu, Xiangxiang 
                AU  - He, Bangshun 
                AU  - Pan, Yuqin 
                AU  - Sun, Huiling 
                AU  - Wang, Shukui 
                TI  - miR-150-5p suppresses tumor progression by targeting VEGFA in colorectal cancer
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101656
                DO  - 10.18632/aging.101656
                SP  - 3421
                EP  - 3437
                PY  - 
                AB  - MicroRNA-150-5p (miR-150-5p) has been implicated in tumor initiation and progression in a variety of cancers. However, its roles in colorectal cancer (CRC) remain largely unknown. In our study, a decreased miR-150-5p expression in CRC tissues was found to be associated with poor overall survival. Moreover, miR-150-5p inhibited CRC cell proliferation, migration, invasion and angiogenesis in vitro and in vivo, and its inhibitory effect could be reversed by transfection of vascular epithelial growth factor A (VEGFA) expression plasmid. Lastly, we demonstrated that miR-150-5p inactivated VEGFA/VEGFR2 and the downstream Akt/mTOR signaling pathway in CRC. Based on these results, we conclude that miR-150-5p may function as a tumor suppressor in CRC, and miR-150-5p/VEGFA axis may be a potential therapeutic target candidate in CRC treatment.
                ER  -

Click to copy this citation from the text box above or download the citation:

Trends in stroke incidence among elderly low-income residents of rural China: a population-based study from 1992 to 2016

Hongyan Lu, Zaiyu Guo, Jie Liu, Heliang Zhang, Wei Zhao, Yanan Wu, Jingxian Ni, Wei Liu, Jun Tu, Jinghua Wang, Xianjia Ning, Jianning Zhang,

https://doi.org/10.18632/aging.101657 pp 3438—3449

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Lu H, Guo Z, Liu J, Zhang H, Zhao W, Wu Y, Ni J, Liu W, Tu J, Wang J, Ning X, Zhang J, . Trends in stroke incidence among elderly low-income residents of rural China: a population-based study from 1992 to 2016. . 10:3438-3449. https://doi.org/10.18632/aging.101657

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Lu, Hongyan 
                AU  - Guo, Zaiyu 
                AU  - Liu, Jie 
                AU  - Zhang, Heliang 
                AU  - Zhao, Wei 
                AU  - Wu, Yanan 
                AU  - Ni, Jingxian 
                AU  - Liu, Wei 
                AU  - Tu, Jun 
                AU  - Wang, Jinghua 
                AU  - Ning, Xianjia 
                AU  - Zhang, Jianning 
                TI  - Trends in stroke incidence among elderly low-income residents of rural China: a population-based study from 1992 to 2016
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101657
                DO  - 10.18632/aging.101657
                SP  - 3438
                EP  - 3449
                PY  - 
                AB  - In China, &gt;70% of stroke deaths occur in people aged ≥65 years. However, trends in the stroke incidence among elderly people are unclear. We aimed to determine trends in the stroke incidence among elderly people in rural China. This was a population-based surveillance study conducted in Tianjin, China. Stroke events and all deaths were registered annually. Trends and annual proportion of change in incidence of first-ever stroke were evaluated from 1992 to 2016. The age-standardized incidence of first-ever stroke increased annually by 3.7% overall in elderly people (2.7% for men; 5.0% for women; all P&lt;0.05). However, from 2008 to 2016, there was no significant change in the trends of stroke incidence among elderly people, across gender and subtypes. The proportion of elderly patients with first-ever stroke decreased by 1.1% annually. In contrast to young patients, annual changes in the incidence of stroke tended to be slight in elderly patients (3.7% vs. 9.5%) with greater increase in female patients than those in male patients (2.7% vs. 10.3% for men; 5.0% vs. 8.9% for women). Thus, the control of risk factors for stroke among elderly people is crucial, especially among older women, to reduce the burden of stroke in China.
                ER  -

Click to copy this citation from the text box above or download the citation:

Transcriptional expressions of Chromobox 1/2/3/6/8 as independent indicators for survivals in hepatocellular carcinoma patients

Gang Ning, Yan-Lin Huang, Li-Min Zhen, Wen-Xiong Xu, Qian Jiao, Fang-Ji Yang, Li-Na Wu, Yong-Yuan Zheng, Jie Song, Yen-Sheng Wang, Chan Xie, Liang Peng,

https://doi.org/10.18632/aging.101658 pp 3450—3473

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Ning G, Huang Y, Zhen L, Xu W, Jiao Q, Yang F, Wu L, Zheng Y, Song J, Wang Y, Xie C, Peng L, . Transcriptional expressions of Chromobox 1/2/3/6/8 as independent indicators for survivals in hepatocellular carcinoma patients. . 10:3450-3473. https://doi.org/10.18632/aging.101658

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Ning, Gang 
                AU  - Huang, Yan-Lin 
                AU  - Zhen, Li-Min 
                AU  - Xu, Wen-Xiong 
                AU  - Jiao, Qian 
                AU  - Yang, Fang-Ji 
                AU  - Wu, Li-Na 
                AU  - Zheng, Yong-Yuan 
                AU  - Song, Jie 
                AU  - Wang, Yen-Sheng 
                AU  - Xie, Chan 
                AU  - Peng, Liang 
                TI  - Transcriptional expressions of Chromobox 1/2/3/6/8 as independent indicators for survivals in hepatocellular carcinoma patients
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101658
                DO  - 10.18632/aging.101658
                SP  - 3450
                EP  - 3473
                PY  - 
                AB  - Chromobox (CBX) proteins are important components of epigenetic regulation complexes known to play key roles in hepatocellular carcinoma (HCC). Little is known about the function of distinct CBXs in HCC. To address this issue, the study investigated the roles of CBXs in the prognosis of HCC using ONCOMINE, UALCAN, Human Protein Atlas, Kaplan-Meier Plotter, c-BioPortal databases. Over expressions of 8 CBXs members were found to be significantly associated with clinical cancer stages and pathological tumor grades in HCC patients. Besides, higher mRNA expressions of CBX1/2/3/6/8 were found to be significantly associated with shorter overall survival (OS) in HCC patients, while higher mRNA expression of CBX7 was associated with favorable OS. Multivariate analysis also showed that high mRNA expressions of CBX1/2/3/6/8 were independent prognostic factors for shorter OS of HCC patients. Moreover, high mutation rate of CBXs (51%) was also observed in HCC patients, and genetic alteration in CBXs was associated with shorter OS and disease-free survival (DFS) in HCC patients. Taken together, these results indicated that CBX1/2/3/6/8 could be prognostic biomarkers for survivals of HCC patients.
                ER  -

Click to copy this citation from the text box above or download the citation:

TGF-β induces corneal endothelial senescence via increase of mitochondrial reactive oxygen species in chronic corneal allograft failure

Zhiyuan Li, Ting Liu, Junwei Ma, Qie Guo, Liang Ma, Qiulan Lv, Yan Jiang, Chao Wei, Jisheng Zhang,

https://doi.org/10.18632/aging.101659 pp 3474—3485

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Li Z, Liu T, Ma J, Guo Q, Ma L, Lv Q, Jiang Y, Wei C, Zhang J, . TGF-β induces corneal endothelial senescence via increase of mitochondrial reactive oxygen species in chronic corneal allograft failure. . 10:3474-3485. https://doi.org/10.18632/aging.101659

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Li, Zhiyuan 
                AU  - Liu, Ting 
                AU  - Ma, Junwei 
                AU  - Guo, Qie 
                AU  - Ma, Liang 
                AU  - Lv, Qiulan 
                AU  - Jiang, Yan 
                AU  - Wei, Chao 
                AU  - Zhang, Jisheng 
                TI  - TGF-β induces corneal endothelial senescence via increase of mitochondrial reactive oxygen species in chronic corneal allograft failure
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101659
                DO  - 10.18632/aging.101659
                SP  - 3474
                EP  - 3485
                PY  - 
                AB  - The corneal endothelium (CE) dysfunction impairs optical transparency and leads to corneal allograft failure. Morphologically, CE cells are characterized by premature senescence at the late stage of corneal graft. However, the detailed molecular mechanisms are largely unknown. Here we found that transforming growth factor-β (TGF-β) is elevated in the CE of late graft failure. In addition, senescence-associated gene p21 and p16 are increased as well, which is consistent with their elevation upon TGF-β treatment in human corneal endothelial cell B4G12. Furthermore, TGF-β treatment leads to high positive ratio of SA-β-gal, indicating B4G12 cells undergo cellular senescence. Mechanistically, we demonstrated that TGF-β could induce mitochondrial ROS (mtROS) production and mtROS scavenger could rescue CE cell senescence upon TGF-β treatment. Our study provides new evidence that elevated TGF-β plays a crucial role in the CE cell senescence and loss in chronic corneal graft failure, which could be potential targets for clinical treatment.
                ER  -

Click to copy this citation from the text box above or download the citation:

Phosphatidylcholine could protect the defect of zearalenone exposure on follicular development and oocyte maturation

Fang-Nong Lai, Xue-Lian Liu, Na Li, Rui-Qian Zhang, Yong Zhao, Yan-Zhong Feng, Charles Martin Nyachoti, Wei Shen, Lan Li,

https://doi.org/10.18632/aging.101660 pp 3486—3506

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Lai F, Liu X, Li N, Zhang R, Zhao Y, Feng Y, Nyachoti CM, Shen W, Li L, . Phosphatidylcholine could protect the defect of zearalenone exposure on follicular development and oocyte maturation. . 10:3486-3506. https://doi.org/10.18632/aging.101660

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Lai, Fang-Nong 
                AU  - Liu, Xue-Lian 
                AU  - Li, Na 
                AU  - Zhang, Rui-Qian 
                AU  - Zhao, Yong 
                AU  - Feng, Yan-Zhong 
                AU  - Nyachoti, Charles Martin 
                AU  - Shen, Wei 
                AU  - Li, Lan 
                TI  - Phosphatidylcholine could protect the defect of zearalenone exposure on follicular development and oocyte maturation
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101660
                DO  - 10.18632/aging.101660
                SP  - 3486
                EP  - 3506
                PY  - 
                AB  - Zearalenone (ZEA) is a well-known exogenous endocrine disruptor and can lead to severe negative effects on the human and animal reproductive process. Using a follicle culture model, we have previously shown that ZEA exposure significantly affected the follicular development and antrum formation but the underlying mechanisms are not well known. Therefore, in this study, we explored the metabolomic changes of granulosa cell (GC) culture media with or without ZEA exposure. The results showed that ZEA significantly increased phosphatidylcholine or phosphatidyl ethanolamine adducts in culture medium. A comprehensive analysis with the metabolome data from follicular fluid of small and large antral follicles showed that lyso phosphatidylcholine (LPC) was accumulated during follicle growth, but was depleted by ZEA exposure. Exogenous supplement with LPC to the follicle growth media or oocyte maturation media can partly protect the defect of ZEA exposure on follicular antrum formation and oocyte maturation. Taken together, our results demonstrate that ZEA exposure hinders the follicular growth and exogenous LPC can practically protect the defect of ZEA on follicular development and oocyte maturation.
                ER  -

Click to copy this citation from the text box above or download the citation:

Angiopoietin-1 and ανβ3 integrin peptide promote the therapeutic effects of L-serine in an amyotrophic lateral sclerosis/Parkinsonism dementia complex model

Hua-ying Cai, Ke-wei Tian, Yuan-yuan Zhang, Hong Jiang, Shu Han,

https://doi.org/10.18632/aging.101661 pp 3507—3527

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Cai H, Tian K, Zhang Y, Jiang H, Han S, . Angiopoietin-1 and ανβ3 integrin peptide promote the therapeutic effects of L-serine in an amyotrophic lateral sclerosis/Parkinsonism dementia complex model. . 10:3507-3527. https://doi.org/10.18632/aging.101661

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Cai, Hua-ying 
                AU  - Tian, Ke-wei 
                AU  - Zhang, Yuan-yuan 
                AU  - Jiang, Hong 
                AU  - Han, Shu 
                TI  - Angiopoietin-1 and ανβ3 integrin peptide promote the therapeutic effects of L-serine in an amyotrophic lateral sclerosis/Parkinsonism dementia complex model
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101661
                DO  - 10.18632/aging.101661
                SP  - 3507
                EP  - 3527
                PY  - 
                AB  - Amyotrophic lateral sclerosis (ALS) is an adult disorder of neurodegeneration that manifests as the destruction of upper and lower motor neurons. Beta-N-methylamino-L-alanine (L-BMAA), an amino acid not present in proteins, was found to cause intraneuronal protein misfolding and to induce ALS/Parkinsonism dementia complex (PDC), which presents symptoms analogous to those of Alzheimer’s-like dementia and Parkinsonism. L-serine suppresses the erroneous incorporation of L-BMAA into proteins in the human nervous system. In this study, angiopoietin-1, an endothelial growth factor crucial for vascular development and angiogenesis, and the integrin αvβ3 binding peptide C16, which inhibits inflammatory cell infiltration, were utilized to improve the local microenvironment within the central nervous system of an ALS/PDC rodent model by minimizing inflammation. Our results revealed that L-serine application yielded better effects than C16+ angiopoietin-1 treatment alone for alleviating apoptotic and autophagic changes and improving cognition and electrophysiological dysfunction, but not for improving the inflammatory micro-environment in the central nerve system, while further advances in attenuating the functional disability and pathological impairment induced by L-BMAA could be achieved by co-treatment with C16 and angiopoietin-1 in addition to L-serine. Therefore, C16+ angiopoietin-1 could be beneficial as a supplement to promote the effects of L-serine treatment.
                ER  -

Click to copy this citation from the text box above or download the citation:

Positive association of familial longevity with the moderate-high HDL-C concentration in Bama Aging Study

Jian Wang, Liwei Shi, Yunfeng Zou, Jiexia Tang, Jiansheng Cai, Yi Wei, Jian Qin, Zhiyong Zhang,

https://doi.org/10.18632/aging.101663 pp 3528—3540

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Wang J, Shi L, Zou Y, Tang J, Cai J, Wei Y, Qin J, Zhang Z, . Positive association of familial longevity with the moderate-high HDL-C concentration in Bama Aging Study. . 10:3528-3540. https://doi.org/10.18632/aging.101663

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Wang, Jian 
                AU  - Shi, Liwei 
                AU  - Zou, Yunfeng 
                AU  - Tang, Jiexia 
                AU  - Cai, Jiansheng 
                AU  - Wei, Yi 
                AU  - Qin, Jian 
                AU  - Zhang, Zhiyong 
                TI  - Positive association of familial longevity with the moderate-high HDL-C concentration in Bama Aging Study
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101663
                DO  - 10.18632/aging.101663
                SP  - 3528
                EP  - 3540
                PY  - 
                AB  - Familial longevity is characterized by beneficial metabolic phenotype in lipid metabolism and APOE genetic variation. Although effects of lipid metabolism and the genetic basis for human longevity remain largely unclear, the contribution of high-density lipoprotein cholesterol (HDL-C) and APOE ε2 allele has been repeatedly demonstrated. This study was designed to determine whether ApoE isoforms and HDL-C levels marked the familial longevity status in an offspring cohort with the age range of 20-89 years old and subsequently to explore the correlation between these two markers and the aging. In the Bama Aging Study (BAS), we recruited 312 offspring from longevity historical families and 298 controls from non-longevity historical families. Information on APOE genotype frequencies, lipid levels, and population characteristics were recorded. No evidence was found to support the association of APOE genotypes with HDL-C and age. HDL-C was significantly higher in longevity group (p &lt; 0.0001). Scatter plot showed a moderately strong linear relationship between the HDL-C level and age in longevity group (r = 0.213, p &lt; 0.001). We conclude that the variation of the APOE gene may not influence familial longevity status at a certain age but the moderate-high HDL-C level contributes to the familial longevity in Bama.
                ER  -

Click to copy this citation from the text box above or download the citation:

Cell and tissue type independent age-associated DNA methylation changes are not rare but common

Tianyu Zhu, Shijie C Zheng, Dirk S. Paul, Steve Horvath, Andrew E. Teschendorff,

https://doi.org/10.18632/aging.101666 pp 3541—3557

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zhu T, Zheng SC, Paul DS, Horvath S, Teschendorff AE, . Cell and tissue type independent age-associated DNA methylation changes are not rare but common. . 10:3541-3557. https://doi.org/10.18632/aging.101666

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Zhu, Tianyu 
                AU  - Zheng, Shijie C 
                AU  - Paul, Dirk S. 
                AU  - Horvath, Steve 
                AU  - Teschendorff, Andrew E. 
                TI  - Cell and tissue type independent age-associated DNA methylation changes are not rare but common
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101666
                DO  - 10.18632/aging.101666
                SP  - 3541
                EP  - 3557
                PY  - 
                AB  - Age-associated DNA methylation changes have been widely reported across many different tissue and cell types. Epigenetic ‘clocks’ that can predict chronological age with a surprisingly high degree of accuracy appear to do so independently of tissue and cell-type, suggesting that a component of epigenetic drift is cell-type independent. However, the relative amount of age-associated DNAm changes that are specific to a cell or tissue type versus the amount that occurs independently of cell or tissue type is unclear and a matter of debate, with a recent study concluding that most epigenetic drift is tissue-specific. Here, we perform a novel comprehensive statistical analysis, including matched multi cell-type and multi-tissue DNA methylation profiles from the same individuals and adjusting for cell-type heterogeneity, demonstrating that a substantial amount of epigenetic drift, possibly over 70%, is shared between significant numbers of different tissue/cell types. We further show that ELOVL2 is not unique and that many other CpG sites, some mapping to genes in the Wnt and glutamate receptor signaling pathways, are altered with age across at least 10 different cell/tissue types. We propose that while most age-associated DNAm changes are shared between cell-types that the putative functional effect is likely to be tissue-specific.
                ER  -

Click to copy this citation from the text box above or download the citation:

Myoblasts rely on TAp63 to control basal mitochondria respiration

Veronica Ciuffoli, Anna Maria Lena, Alessandra Gambacurta, Gerry Melino, Eleonora Candi,

https://doi.org/10.18632/aging.101668 pp 3558—3573

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Ciuffoli V, Lena AM, Gambacurta A, Melino G, Candi E, . Myoblasts rely on TAp63 to control basal mitochondria respiration. . 10:3558-3573. https://doi.org/10.18632/aging.101668

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Ciuffoli, Veronica 
                AU  - Lena, Anna Maria 
                AU  - Gambacurta, Alessandra 
                AU  - Melino, Gerry 
                AU  - Candi, Eleonora 
                TI  - Myoblasts rely on TAp63 to control basal mitochondria respiration
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101668
                DO  - 10.18632/aging.101668
                SP  - 3558
                EP  - 3573
                PY  - 
                AB  - p53, with its family members p63 and p73, have been shown to promote myoblast differentiation by regulation of the function of the retinoblastoma protein and by direct activation of p21Cip/Waf1 and p57Kip2, promoting cell cycle exit. In previous studies, we have demonstrated that the TAp63γ isoform is the only member of the p53 family that accumulates during in vitro myoblasts differentiation, and that its silencing led to delay in myotube fusion. To better dissect the role of TAp63γ in myoblast physiology, we have generated both sh-p63 and Tet-On inducible TAp63γ clones. Gene array analysis of sh-p63 C2C7 clones showed a significant modulation of genes involved in proliferation and cellular metabolism. Indeed, we found that sh-p63 C2C7 myoblasts present a higher proliferation rate and that, conversely, TAp63γ ectopic expression decreases myoblasts proliferation, indicating that TAp63γ specifically contributes to myoblasts proliferation, independently of p53 and p73. In addition, sh-p63 cells have a defect in mitochondria respiration highlighted by a reduction in spare respiratory capacity and a decrease in complex I, IV protein levels. These results demonstrated that, beside contributing to cell cycle exit, TAp63γ participates to myoblasts metabolism control.
                ER  -

Click to copy this citation from the text box above or download the citation:

Suppression of mTORC1 activity in senescent Ras-transformed cells neither restores autophagy nor abrogates apoptotic death caused by inhibition of MEK/ERK kinases

Elena Y. Kochetkova, Galina I. Blinova, Olga A. Bystrova, Marina G. Martynova, Valeriy A. Pospelov, Tatiana V. Pospelova,

https://doi.org/10.18632/aging.101686 pp 3574—3589

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Kochetkova EY, Blinova GI, Bystrova OA, Martynova MG, Pospelov VA, Pospelova TV, . Suppression of mTORC1 activity in senescent Ras-transformed cells neither restores autophagy nor abrogates apoptotic death caused by inhibition of MEK/ERK kinases. . 10:3574-3589. https://doi.org/10.18632/aging.101686

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Kochetkova, Elena Y. 
                AU  - Blinova, Galina I. 
                AU  - Bystrova, Olga A. 
                AU  - Martynova, Marina G. 
                AU  - Pospelov, Valeriy A. 
                AU  - Pospelova, Tatiana V. 
                TI  - Suppression of mTORC1 activity in senescent Ras-transformed cells neither restores autophagy nor abrogates apoptotic death caused by inhibition of MEK/ERK kinases
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101686
                DO  - 10.18632/aging.101686
                SP  - 3574
                EP  - 3589
                PY  - 
                AB  - Autophagy is conservative catabolic process that degrades organelles, in particular, mitochondria, and misfolded proteins within the lysosomes, thus maintaining cellular viability. Despite the close relationship between mitochondrial dysfunction and cellular senescence, it is unclear how mitochondria damage can induce autophagy in senescent cells. We show that MEK/ERK suppression induces mitochondria damage followed by apoptosis of senescent Ras-expressing cells. To understand the role of persistent mTORC1 signaling in breaking the cAMPK-induced autophagy caused by mitochondrial damage, we inhibited mTORС1 with low concentrations of pp242. mTORC1 suppression neither restores the AMPK-induced autophagy nor decreases the level of apoptosis upon MEK/ERK inhibition. We discovered the existence of an alternative autophagy-like way that partially increases the viability of senescent cells under suppressed mTORC1. The pp242-treated cells survive due to formation of the non-autophagous LC3-negative vacuoles, which contain the damaged mitochondria and lysosomes with the following excretion the content from the cell. MEK/ERK activity is required to implement this process in senescent cells. Senescent cells exhibit distinctive spatial distribution of organelles and proteins that provides uncoupling of final participants of autophagy. We show that this feature stops the process of cytoprotective autophagy in response to MEK/ERK suppression, thus allowing selective elimination of senescent Ras-expressing cells.
                ER  -

Click to copy this citation from the text box above or download the citation:

The senescent cell epigenome

Na Yang, Payel Sen,

https://doi.org/10.18632/aging.101617 pp 3590—3609

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Yang N, Sen P, . The senescent cell epigenome. . 10:3590-3609. https://doi.org/10.18632/aging.101617

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Yang, Na 
                AU  - Sen, Payel 
                TI  - The senescent cell epigenome
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101617
                DO  - 10.18632/aging.101617
                SP  - 3590
                EP  - 3609
                PY  - 
                AB  -  A critical hallmark of aging is cellular senescence, a state of growth arrest and inflammatory cytokine release in cells, caused by a variety of stresses. Recent work has convincingly linked the accumulation of senescent cells in aged tissues to a decline in health and a limit of lifespan, primarily through "inflammaging". Importantly, interventions that clear senescent cells have achieved marked improvements in healthspan and lifespan in mice. A growing list of studies show that environmental stimuli can affect aging and longevity through conserved pathways which, in turn, modulate chromatin states. This review consolidates key findings of chromatin state changes in senescence including histone modifications, histone variants, DNA methylation and changes in three-dimensional genome organization. This information will facilitate the identification of mechanisms and discovery of potential epigenetic targets for therapeutic interventions in aging and age-related disease.
                ER  -

Click to copy this citation from the text box above or download the citation:

Accelerated aging in perinatally HIV-infected children: clinical manifestations and pathogenetic mechanisms

Elena Chiappini, Martina Bianconi, Annalisa Dalzini, Maria Raffaella Petrara, Luisa Galli, Carlo Giaquinto, Anita De Rossi,

https://doi.org/10.18632/aging.101622 pp 3610—3625

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Chiappini E, Bianconi M, Dalzini A, Petrara MR, Galli L, Giaquinto C, De Rossi A, . Accelerated aging in perinatally HIV-infected children: clinical manifestations and pathogenetic mechanisms. . 10:3610-3625. https://doi.org/10.18632/aging.101622

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Chiappini, Elena 
                AU  - Bianconi, Martina 
                AU  - Dalzini, Annalisa 
                AU  - Petrara, Maria Raffaella 
                AU  - Galli, Luisa 
                AU  - Giaquinto, Carlo 
                AU  - De Rossi, Anita 
                TI  - Accelerated aging in perinatally HIV-infected children: clinical manifestations and pathogenetic mechanisms
                JO  - 
                JA  - 
                VL  - 10
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101622
                DO  - 10.18632/aging.101622
                SP  - 3610
                EP  - 3625
                PY  - 
                AB  - Background: Premature aging and related diseases have been documented in HIV-infected adults. Data are now emerging also regarding accelerated aging process in HIV-infected children.Methods: A narrative review was performed searching studies on PubMed published in English language in 2004-2017, using appropriate key words, including “aging”, “children”, “HIV”, “AIDS”, “immunosenescence”, “pathogenesis”, “clinical conditions”.Results: Premature immunosenescence phenotype of B and T cells in HIV-infected children is mediated through immune system activation and chronic inflammation. Ongoing inflammation processes have been documented by increased levels of pathogen-associated molecular patterns (PAMPS), increased mitochondrial damage, higher levels of pro-inflammatory cytokines, and a positive correlation between sCD14 levels and percentages of activated CD8+ cells. Other reported features of premature aging include cellular replicative senescence, linked to an accelerated telomeres shortening. Finally, acceleration of age-associated methylation pattern and other epigenetic modifications have been described in HIV-infected children. All these features may favor the clinical manifestations related to premature aging. Lipid and bone metabolism, cancers, cardiovascular, renal, and neurological systems should be carefully monitored, particularly in children with detectable viremia and/or with CD4/CD8 ratio inversion.Conclusion: Aging processes in children with HIV infection impact their quality and length of life. Further studies regarding the mechanisms involved in premature aging are needed to search for potential targets of treatment.
                ER  -

Click to copy this citation from the text box above or download the citation:

Correction: MicroRNA-939 inhibits cell proliferation via targeting LRSAM1 in Hirschsprung’s disease

Guanglin Chen, Chunxia Du, Ziyang Shen, Lei Peng, Hua Xie, Rujin Zang, Hongxing Li, Yankai Xia, Weibing Tang,

https://doi.org/10.18632/aging.101650 pp 3626

PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Chen G, Du C, Shen Z, Peng L, Xie H, Zang R, Li H, Xia Y, Tang W, . Correction: MicroRNA-939 inhibits cell proliferation via targeting LRSAM1 in Hirschsprung’s disease. . 10:3626-3626. https://doi.org/10.18632/aging.101650

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Click to copy this citation from the text box above or download the citation:

Correction: CD40L promotes development of acute aortic dissection via induction of inflammation and impairment of endothelial cell function

Lu Han, Lu Dai, Yuan-Fei Zhao, Hai-Yang Li, Ou Liu, Feng Lan, Wen-Jian Jiang, Hong-Jia Zhang,

https://doi.org/10.18632/aging.101651 pp 3627

PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Han L, Dai L, Zhao Y, Li H, Liu O, Lan F, Jiang W, Zhang H, . Correction: CD40L promotes development of acute aortic dissection via induction of inflammation and impairment of endothelial cell function. . 10:3627-3627. https://doi.org/10.18632/aging.101651

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Click to copy this citation from the text box above or download the citation:

Volume 10, Issue 11

About the Cover

Editorials

Nienke M. van Loon, Patrick C.N. Rensen, Noam Zelcer,

Cite this Article

How to cite

Copy or Download citation:

Rocco A. Montone, Michele Russo, Giampaolo Niccoli,

Cite this Article

How to cite

Copy or Download citation:

Allison B. Herman, Michael V. Autieri,

Cite this Article

How to cite

Copy or Download citation:

Sofia Chatzidou, Georgios Georgiopoulos, Christos Kontogiannis,

Cite this Article

How to cite

Copy or Download citation:

Jan Laczó, Martina Parizkova, Scott D. Moffat,

Cite this Article

How to cite

Copy or Download citation:

Jose J. Lopez, Isaac Jardin, Juan A. Rosado,

Cite this Article

How to cite

Copy or Download citation:

Hansjörg Schwertz, Matthew T. Rondina,

Cite this Article

How to cite

Copy or Download citation:

Olalla Pancorbo, David Rodriguez-Luna,

Cite this Article

How to cite

Copy or Download citation:

Daniel Ferreira, Lars-Olof Wahlund, Eric Westman,

Cite this Article

How to cite

Copy or Download citation:

Ana M. Valdes, Cristina Menni,

Cite this Article

How to cite

Copy or Download citation:

Elena Anahi Bignante, Alfredo Lorenzo,

Cite this Article

How to cite

Copy or Download citation:

Aiste Steponenaite, Stephany M. Biello, Gurprit S. Lall,

Cite this Article

How to cite

Copy or Download citation:

Theory Article

Mikhail V. Blagosklonny,

Cite this Article

How to cite

Copy or Download citation:

Meeting Report

Cite this Article

How to cite

Copy or Download citation:

Research Papers

Le Li, Yi Chen, Changchi Chenzhao, Shuxiang Fu, Qumiao Xu, Jinfeng Zhao,

Cite this Article

How to cite

Copy or Download citation:

Yabin Gong, Zhilong Zhang, Zhanglin Chang, Hao Zhou, Ruqian Zhao, Bin He,

Cite this Article

How to cite

Copy or Download citation:

Chen-Di Lu, Ji-Kang Ma, Zheng-Yang Luo, Qun-Xi Tai, Pu Wang, Pei-Pei Guan,

Cite this Article

How to cite

Copy or Download citation:

Xian-tao Wang, Xiao-dan Wu, Yuan-xi Lu, Yu-han Sun, Han-hua Zhu, Jia-bao Liang, Wen-kai He, Lang Li,

Cite this Article

How to cite

Copy or Download citation:

Isabella Zironi, Entelë Gavoçi, Giovanna Lattanzi, Angela Virelli, Fabrizio Amorini, Daniel Remondini, Gastone Castellani,

Cite this Article

How to cite