Cell Science

Aging (Aging-US)

Aging-US published this trending editorial on July 19, 2022 in Volume 14, Issue 14, entitled, "Restoring rhythm to prevent age-related fractures” by researchers Annelies E. Smit, Maaike Schilperoort, and Elizabeth M. Winter from the Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands.

DOI - https://doi.org/10.18632/aging.204192 (PDF Download)

Corresponding author - Elizabeth M. Winter - e.m.winter@lumc.nl

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Keywords - aging, circadian rhythm, fractures, osteoporosis, glucocorticoids, chronotherapy

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at https://www.Aging-US.com​​ and connect with us:

SoundCloud - https://soundcloud.com/Aging-Us
Facebook - https://www.facebook.com/AgingUS/
Twitter - https://twitter.com/AgingJrnl
Instagram - https://www.instagram.com/agingjrnl/
YouTube - https://www.youtube.com/agingus​
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Trending With Impact: Restoring Rhythm to Prevent Age-related Fractures

Aging-US published this research paper on July 5, 2022 in Volume 14, Issue 14, entitled, "Common electrocardiogram measures are not associated with telomere length" by researchers Department of Cardiology, University Hospital, LMU Munich, Munich, Germany; German Centre for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany; Institute of Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany; Research Unit Molecular Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany; Institute for Medical Information Processing, Biometry and Epidemiology, Medical Faculty, LMU Munich, Munich, Germany; Institute of Genetic Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany; Institute of Medical Biostatistics, Epidemiology and Informatics (IMBEI), University Medical Center, Johannes Gutenberg University, Mainz, Germany; Pettenkofer School of Public Health Munich, Institute for Medical Information Processing, Biometry and Epidemiology, Medical Faculty, LMU Munich, Munich, Germany.

DOI - https://doi.org/10.18632/aging.204149

Corresponding author - Moritz F. Sinner - moritz.sinner@med.uni-muenchen.de

Abstract

Aims: Aging is accompanied by telomere shortening. Increased telomere shortening is considered a marker of premature aging. Cardiac aging results in the development of cardiac pathologies. Electrocardiogram (ECG) measures reflect cardiac excitation, conduction, and repolarization. ECG measures also prolong with aging and are associated with cardiac pathologies including atrial fibrillation. As premature prolongation of ECG measures is observed, we hypothesized that such prolongation may be associated with telomere length.

Methods and Results: We studied the large, community-based KORA F4 Study. Of 3,080 participants enrolled between 2006 and 2007 with detailed information on demographic, anthropometric, clinical, and ECG characteristics, 2,575 presented with available data on leukocyte telomere length. Telomere length was determined by real-time quantitative PCR and expressed relative to a single copy gene. We fitted multivariable adjusted linear regression models to associate the ECG measures RR-interval, PR-interval, QRS-duration, and heart rate corrected QTc with telomere length.

In our cohort, the mean age was 54.9±12.9 years and 46.6% were men. Increased age was associated with shorter telomere length (p<0.01), and men had shorter telomere length than women (p<0.05). In unadjusted models, heart rate (p=0.023), PR-interval (p<0.01), and QTc-interval (p<0.01) were significantly associated with shorter telomere length. However, no significant associations remained after accounting for age, sex, and covariates.

Conclusions: ECG measures are age-dependent, but not associated with shortened telomere length as a marker of biological aging. Further research is warranted to clarify if shortened telomeres are associated with clinical cardiac pathologies including atrial fibrillation.

Keywords - aging, electrocardiogram, telomere length, cardiac aging

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at https://www.Aging-US.com​​ and connect with us:

SoundCloud - https://soundcloud.com/Aging-Us
Facebook - https://www.facebook.com/AgingUS/
Twitter - https://twitter.com/AgingJrnl
Instagram - https://www.instagram.com/agingjrnl/
YouTube - https://www.youtube.com/agingus​
LinkedIn - https://www.linkedin.com/company/aging/
Pinterest - https://www.pinterest.com/AgingUS/

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Paper Spotlight: Common ECG Measures are not Associated with Telomere Length

In the second installment of the Longevity & Aging Series, Dr. Steve Horvath revisits papers he co-authored that were published by Aging (Aging-US) and featured as a special collection of his research.

Special Collection - https://www.aging-us.com/special-collections-archive/steve-horvath
Author contact - Steve Horvath - shorvath@mednet.ucla.edu

Papers - 

DNA-methylation-based telomere length estimator: comparisons with measurements from flow FISH and qPCR
https://doi.org/10.18632/aging.203126

Epigenetic mutation load is weakly correlated with epigenetic age acceleration
https://doi.org/10.18632/aging.103950

Blood DNA methylation sites predict death risk in a longitudinal study of 12, 300 individuals
https://doi.org/10.18632/aging.103408

Epigenome-wide association study of leukocyte telomere length
https://doi.org/10.18632/aging.102230

DNA methylation-based estimator of telomere length
https://doi.org/10.18632/aging.102173

Optimism is not associated with two indicators of DNA methylation aging
https://doi.org/10.18632/aging.102090

Placental epigenetic clocks: estimating gestational age using placental DNA methylation levels
https://doi.org/10.18632/aging.102049

Rapamycin retards epigenetic ageing of keratinocytes independently of its effects on replicative senescence, proliferation and differentiation
https://doi.org/10.18632/aging.101976

Epigenetic clock analysis of human fibroblasts in vitro: effects of hypoxia, donor age, and expression of hTERT and SV40 largeT
https://doi.org/10.18632/aging.101955

DNA methylation GrimAge strongly predicts lifespan and healthspan
https://doi.org/10.18632/aging.101684

Cell and tissue type independent age-associated DNA methylation changes are not rare but common
https://doi.org/10.18632/aging.101666

A multi-tissue full lifespan epigenetic clock for mice
https://doi.org/10.18632/aging.101590

Epigenetic ageing is distinct from senescence-mediated ageing and is not prevented by telomerase expression
https://doi.org/10.18632/aging.101588

Epigenetic clock for skin and blood cells applied to Hutchinson Gilford Progeria Syndrome and ex vivo studies
https://doi.org/10.18632/aging.101508

An epigenetic biomarker of aging for lifespan and healthspan
https://doi.org/10.18632/aging.101414

Leukocyte telomere length, T cell composition and DNA methylation age
https://doi.org/10.18632/aging.101293

Accelerated epigenetic aging in Werner syndrome
https://doi.org/10.18632/aging.101217

An epigenetic aging clock for dogs and wolves
https://doi.org/10.18632/aging.101211

Longitudinal study of surrogate aging measures during human immunodeficiency virus seroconversion
https://doi.org/10.18632/aging.101184

Epigenetic clock analysis of diet, exercise, education, and lifestyle factors
https://doi.org/10.18632/aging.101168

Specific premature epigenetic aging of cartilage in osteoarthritis
https://doi.org/10.18632/aging.101053

DNA methylation-based measures of biological age: meta-analysis predicting time to death
https://doi.org/10.18632/aging.101020

Huntington's disease accelerates epigenetic aging of human brain and disrupts DNA methylation levels
https://doi.org/10.18632/aging.101005

Epigenetic age of the pre-frontal cortex is associated with neuritic plaques, amyloid load, and Alzheimer’s disease related cognitive functioning
https://doi.org/10.18632/aging.100864

Decreased epigenetic age of PBMCs from Italian semi-supercentenarians and their offspring
https://doi.org/10.18632/aging.100861

Increased epigenetic age and granulocyte counts in the blood of Parkinson's disease patients
https://doi.org/10.18632/aging.100859

DNA methylation age of blood predicts future onset of lung cancer in the women's health initiative
https://doi.org/10.18632/aging.100809

Epigenetic age analysis of children who seem to evade aging
https://doi.org/10.18632/aging.100744

The cerebellum ages slowly according to the epigenetic clock
https://doi.org/10.18632/aging.100742

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at https://www.Aging-US.com​​ or connect with us:

SoundCloud - https://soundcloud.com/Aging-Us
Facebook - https://www.facebook.com/AgingUS/
Twitter - https://twitter.com/AgingJrnl
Instagram - https://www.instagram.com/agingjrnl/
YouTube - https://www.youtube.com/agingus​
LinkedIn - https://www.linkedin.com/company/aging/
Pinterest - https://www.pinterest.com/AgingUS/

Longevity & Aging Series (EP 2): Dr. Steve Horvath’s Special Collection in Aging

Oncotarget

Oncotarget published this research paper on July 28, 2022 in Volume 13, entitled, "Diverse geroprotectors differently affect a mechanism linking cellular aging to cellular quiescence in budding yeast" by researchers from the Department of Biology, Concordia University, Montreal, Quebec H4B 1R6, Canada.

DOI - https://doi.org/10.18632/oncotarget.28256

Correspondence to - Vladimir I. Titorenko - vladimir.titorenko@concordia.ca

Abstract

We propose a hypothesis of a mechanism linking cellular aging to cellular quiescence in chronologically aging budding yeast. Our hypothesis posits that this mechanism integrates four different processes, all of which are initiated after yeast cells cultured in a medium initially containing glucose consume it. Quiescent cells that develop in these cultures can be separated into the high- and low-density sub-populations of different buoyant densities. Process 1 of the proposed mechanism consists of a cell-cycle arrest in the G1 phase and leads to the formation of high-density quiescent cells. Process 2 results in converting high-density quiescent cells into low-density quiescent cells. Processes 3 and 4 cause a fast or slow decline in the quiescence of low- or high-density quiescent cells, respectively. Here, we tested our hypothesis by assessing how four different geroprotectors influence the four processes that could link cellular aging to cellular quiescence. We found that these geroprotectors differently affect processes 1 and 2 and decelerate processes 3 and 4. We also found that a rise in trehalose within quiescent yeast contributes to chronological aging and quiescence maintenance. These data collectively provide conclusive evidence for a mechanistic link between cellular aging and cellular quiescence.

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Keywords - cellular aging, cellular quiescence, longevity, gerotargets, geroprotectors

About Oncotarget

Oncotarget is a peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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Diverse Geroprotectors Differently Affect Mechanism Linking Cellular Aging to Cellular Quiescence in Budding Yeast

Aging-US published this trending research paper on July 8, 2022 in Volume 14, Issue 14, entitled, "Short-term resveratrol treatment restored the quality of oocytes in aging mice" by researchers from the Department of Obstetrics and Gynecology, International University of Health and Welfare School of Medicine, Chiba 286-8686, Japan; Department of Biodesign, Institute of Biomaterials and Bioengineering, Tokyo Medical and Dental University Chiyoda-ku, Tokyo 101-0062, Japan; Department of Obstetrics and Gynecology, Juntendo University Faculty of Medicine Bunkyo-ku, Tokyo 113-8421, Japan; Aging Stress Response Project Team, National Center for Geriatrics and Gerontology, Obu, Aichi 474-8511, Japan.

DOI - https://doi.org/10.18632/aging.204157

Corresponding author - Kazuhiro Kawamura - k.kawamura.aq@juntendo.ac.jp

Abstract

The quality of oocytes declines by aging, resulting in their low competences for fertility. Here, resveratrol treatment showed increases in the rates of implantation and live offspring as well as decreases in the abortion rate as short as one week after treatment, although the number of ovulated oocytes and the rates of fertilization and blastocyst formation were not changed following resveratrol treatment. Resveratrol treatment did not cause abnormalities mouse estrous cycles and body weights. No abnormality was detected in both fetuses and placentas after 22 weeks of resveratrol treatment and the fetuses had normal fertility. Positive correlations were found between serum resveratrol levels and pregnancy and live offspring rates as well as ovarian expression levels of Sirt1, Sirt3, Sirt4, Sirt5, and Sirt7. The mitochondrial membrane potential and ATP content but not copy number of mitochondrial DNA in oocytes was increased in aging mice with resveratrol treatment. In conclusion, we demonstrated the restoration of oocyte quality in aging mice in addition to the prevention of their quality decline during aging by restoring mitochondrial functions by resveratrol treatment without adverse effects in the animals and their offspring.

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Keywords - aging, resveratrol, age-associated infertility, oocyte quality, Sirtuin, mitochondria

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at https://www.Aging-US.com​​ and connect with us:

SoundCloud - https://soundcloud.com/Aging-Us
Facebook - https://www.facebook.com/AgingUS/
Twitter - https://twitter.com/AgingJrnl
Instagram - https://www.instagram.com/agingjrnl/
YouTube - https://www.youtube.com/agingus​
LinkedIn - https://www.linkedin.com/company/aging/
Pinterest - https://www.pinterest.com/AgingUS/

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Trending With Impact: Resveratrol Treatment Restored Quality of Oocytes in Aging Mice

Dr. Cristina Aguayo-Mazzucato from Beta Cell Aging Lab, Joslin Diabetes Center, Harvard Medical School, discusses an editorial she co-authored that was published by Aging (Aging-US) in Volume 14, Issue 11, entitled, “Biological age in diabetes and precision medicine.”

DOI - https://doi.org/10.18632/aging.204123

Corresponding author - Cristina Aguayo-Mazzucato - cristina.aguayo-mazzucato@joslin.harvard.edu

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Keywords - biological age, diabetes mellitus, chronological age, DNA methylation, clinical biomarkers

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at http://www.Aging-US.com​​ or connect with us:

SoundCloud - https://soundcloud.com/Aging-Us
Facebook - https://www.facebook.com/AgingUS/
Twitter - https://twitter.com/AgingJrnl
Instagram - https://www.instagram.com/agingjrnl/
YouTube - https://www.youtube.com/agingus​
LinkedIn - https://www.linkedin.com/company/aging/
Pinterest - https://www.pinterest.com/AgingUS/

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Behind the Study: Biological Age in Diabetes and Precision Medicine

Oncotarget published this trending research paper on July 19, 2022 in Volume 13, entitled, "CUDC907, a dual phosphoinositide-3 kinase/histone deacetylase inhibitor, promotes apoptosis of NF2 Schwannoma cells" by researchers from the Burnett School of Biomedical Sciences, College of Medicine, University of Central Florida, Orlando, FL; Department of Otolaryngology, University of Miami Miller School of Medicine, Miami, FL; John P. Hussman Institute for Human Genomics, University of Miami Miller School of Medicine, Miami, FL; Department of Pathology, University of Miami Miller School of Medicine, Miami, FL; Department of Human Genetics, University of Miami Miller School of Medicine, Miami, FL.

DOI - https://doi.org/10.18632/oncotarget.28254

Correspondence to - Cristina Fernandez-Valle - cfv@ucf.edu

Abstract

Neurofibromatosis Type 2 (NF2) is a rare tumor disorder caused by pathogenic variants of the merlin tumor suppressor encoded by NF2. Patients develop vestibular schwannomas (VS), peripheral schwannomas, meningiomas, and ependymomas. There are no approved drug therapies for NF2. Previous work identified phosphoinositide-3 kinase (PI3K) as a druggable target. Here we screened PI3K pathway inhibitors for efficacy in reducing viability of human schwannoma cells. The lead compound, CUDC907, a dual histone deacetylase (HDAC)/PI3K inhibitor, was further evaluated for its effects on isolated and nerve-grafted schwannoma model cells, and primary VS cells. CUDC907 (3 nM IG50) reduced human merlin deficient Schwann cell (MD-SC) viability and was 5–100 fold selective for MD over WT-SCs. CUDC907 (10 nM) promoted cell cycle arrest and caspase-3/7 activation within 24 h in human MD-SCs. Western blots confirmed a dose-dependent increase in acetylated lysine and decreases in pAKT and YAP. CUDC907 decreased tumor growth rate by 44% in a 14-day treatment regimen, modulated phospho-target levels, and decreased YAP levels. In five primary VS, CUDC907 decreased viability, induced caspase-3/7 cleavage, and reduced YAP levels. Its efficacy correlated with basal phospho-HDAC2 levels. CUDC907 has cytotoxic activity in NF2 schwannoma models and primary VS cells and is a candidate for clinical trials.

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Press release - https://www.oncotarget.com/news/pr/oncotarget-cudc-promotes-apoptosis-of-nf-schwannoma-cells/

Keywords - fimepinostat, Schwann cell, vestibular schwanomma, merlin, nerve allograft

About Oncotarget

Oncotarget is a peer-reviewed, open access biomedical journal covering research on all aspects of oncology.

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Trending With Impact: CUDC907 Promotes Apoptosis of NF2 Schwannoma Cells

JMIR Publications

JMIR Publications recently published “Establishing Institutional Scores With the Rigor and Transparency Index: Large-scale Analysis of Scientific Reporting Quality” in the Journal of Medical Internet Research (JMIR), which reported that improving rigor and transparency measures should lead to improvements in reproducibility across the scientific literature, but assessing measures of transparency tends to be very difficult if performed manually by reviewers.

The overall aim of this study is to establish a scientific reporting quality metric that can be used across institutions and countries, as well as to highlight the need for high-quality reporting to ensure replicability within biomedicine, making use of manuscripts from the Reproducibility Project: Cancer Biology.

The authors address an enhancement of the previously introduced Rigor and Transparency Index (RTI), which attempts to automatically assess the rigor and transparency of journals, institutions, and countries using manuscripts scored on criteria found in reproducibility guidelines (eg, NIH, MDAR, ARRIVE).

Using work by the Reproducibility Project: Cancer Biology, the authors could determine that replication studies scored significantly higher than the original papers which, according to the project, all required additional information from authors to begin replication efforts.

Unfortunately, RTI measures for journals, institutions, and countries all currently score lower than the replication study average. If they take the RTI of these replication studies as a target for future manuscripts, more work will be needed to ensure the average manuscript contains sufficient information for replication attempts.

Dr. Anita Bandrowski from the University of California San Diego said, "Research reproducibility is necessary for scientific progress. However, over the last decade, numerous reports on research irreproducibility have shed light on a lingering problem, one that is proving to be both troublesome and costly."

In an effort to encourage reproducibility, numerous scientific organizations and journals have adopted the Transparency and Openness Promotion guidelines, which focus on establishing best practices at the level of individual journals.

Along a similar vein, the publisher-driven Materials Design, Analysis, and Reporting framework is a multidisciplinary research framework designed to improve reporting transparency across life science research at the level of individual manuscripts.

This framework provides a consistent, minimum reporting checklist whose criteria were used, in part, to create the first RTI, a journal quality metric focusing on research methodologies and reporting transparency.

Specifically, the authors here introduce the latest version of the RTI, which represents the mean SciScore over a subset of papers, and demonstrate how it can be used to assess reporting transparency within research institutions.

While we cannot simply describe all papers scoring a “2” as not replicable and all papers scoring an “8” as replicable, as numerous fields and their subsequent best practices exist, we can state that higher scores are associated with more methodological detail and as such are likely easier to use to attempt a replication. 

DOI - https://doi.org/10.2196/37324
Full-text - https://www.jmir.org/2022/6/e37324
Free Altmetric Report - https://jmir.altmetric.com/details/13...

JMIR Publications is a leading, born-digital, open access publisher of 30+ academic journals and other innovative scientific communication products that focus on the intersection of health and technology. Its flagship journal, the Journal of Medical Internet Research, is the leading digital health journal globally in content breadth and visibility, and it is the largest journal in the medical informatics field.

To learn more about JMIR Publications, please visit https://www.JMIRPublications.com 

SciScore is a scientific content checker / validation tool that verifies common rigor criteria (NIH, MDAR, ARRIVE) and research resources (antibodies, cell lines, organisms). These guidelines can be checked by editorial, but the process is tedious and takes a lot of effort from a skilled professional, so checklists are enforced only in the best-resourced journals. SciScore uses text mining techniques to do the job in minutes, providing a report to the editors, reviewers or authors about criteria that have and have not been addressed. Furthermore, it provides a numerical score, which allows editors to assess the percentage of criteria met or not met at a glance.
 
Researchers: Anita Bandrowski | anita@scicrunch.com
Media/Publishers: Martijn Roelandse | martijn@martijnroelandse.dev

Journal of Medical Internet Research | Rigor & Transparency Analysis of Scientific Reporting Quality

Aging-US published this research paper on July 12, 2022 in Volume 14, Issue 13, entitled, "Age-related neuroendocrine, cognitive, and behavioral co-morbidities are promoted by HIV-1 Tat expression in male mice" by researchers from Department of BioMolecular Sciences, School of Pharmacy, University of Mississippi, University, MS; Department of Psychiatry, McLean Imaging Center, McLean Hospital/Harvard Medical School, Belmont, MA; Research Institute of Pharmaceutical Sciences, University of Mississippi, University, MS.

DOI - https://doi.org/10.18632/aging.204166

Corresponding author - Jason J. Paris - parisj@olemiss.edu

Abstract

In the U.S. about half of the HIV-infected individuals are aged 50 and older. In men living with HIV, secondary hypogonadism is common and occurs earlier than in seronegative men, and its prevalence increases with age. While the mechanisms(s) are unknown, the HIV-1 trans-activator of transcription (Tat) protein disrupts neuroendocrine function in mice partly by dysregulating mitochondria and neurosteroidogenesis. We hypothesized that conditional Tat expression in middle-aged male transgenic mice [Tat(+)] would promote age-related comorbidities compared to age-matched controls [Tat(−)]. We expected Tat to alter steroid hormone milieu consistent with behavioral deficits. Middle-aged Tat(+) mice had lower circulating testosterone and progesterone than age-matched controls and greater circulating corticosterone and central allopregnanolone than other groups. Young Tat(+) mice had greater circulating progesterone and estradiol-to-testosterone ratios. Older age or Tat exposure increased anxiety-like behavior (open field; elevated plus-maze), increased cognitive errors (radial arm water maze), and reduced grip strength. Young Tat(+), or middle-aged Tat(−), males had higher mechanical nociceptive thresholds than age-matched counterparts. Steroid levels correlated with behaviors. Thus, Tat may contribute to HIV-accelerated aging.

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Keywords - aging, hypothalamic-pituitary-adrenal axis, hypothalamic-pituitary-gonadal axis, secondary hypogonadism, trans-activating transcriptor

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at https://www.Aging-US.com​​ and connect with us:

SoundCloud - https://soundcloud.com/Aging-Us
Facebook - https://www.facebook.com/AgingUS/
Twitter - https://twitter.com/AgingJrnl
Instagram - https://www.instagram.com/agingjrnl/
YouTube - https://www.youtube.com/agingus​
LinkedIn - https://www.linkedin.com/company/aging/
Pinterest - https://www.pinterest.com/AgingUS/

Aging-US is published by Impact Journals, LLC: http://www.ImpactJournals.com​​

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