Aging-US

Aging-US published "Identification of RNA binding protein interacting with circular RNA and hub candidate network for hepatocellular carcinoma" which reported that 17 DERBPs, which were commonly dysregulated in HCC from The Clinical Proteomic Tumor Analysis Consortium, The Cancer Genome Atlas and International Cancer Genome Consortium projects, were utilized to construct the RBP-circRNA network.

Additionally, gene set enrichment analysis showed that dysregulated TARDBP might be involved in some pathways related to the HCC pathogenesis.

Therefore, a hub RBP-circRNA network was generated based on TARDBP.

RNA immunoprecipitation and RNA pull-down confirmed that hsa_circ_0004913 binds to TARDBP.

These findings, published in Aging-US, indicated a certain RBP-circRNA regulatory network potentially involved in the pathogenesis of HCC, which provides novel insights into the mechanism of study and biomarker identification for HCC.

Dr. Yuhan Chen from The Southern Medical University said, "Hepatocellular carcinoma (HCC) is most common types of primary liver cancer."

Previous studies have demonstrated that circRNAs can act as sponges of RNA binding protein, in the meantime RBPs are also able to participate in back-splicing. Therefore, the interaction with RBPs can be also regarded as a crucial element to explore functions of circRNAs.

However, there are very few studies related to the effects of RBP-circRNA interactions on HCC, which requires more exploration.

In this study, the authors screened out the differently expressed circRNA in HCC cases from Gene Expression Omnibus database and predicted the RBPs binding to DEcircRNA.

After evaluating the expression level of RBPs in HCC from The Clinical Proteomic Tumor Analysis Consortium, International Cancer Genome Consortium and The Cancer Genome Atlas projects, they utilized 17 common DERBPs to construct the RBP-circRNA regulatory network in HCC.

These findings indicated that certain RBP-circRNA networks may be closely related to HCC, which provides ideas for the mechanism of study for HCC.

The Chen Research Team concluded in their Aging-US Research Output, "we identified some DERBPs interacting with circRNAs and generated RBP-circRNA regulatory networks for HCC. Among the DERBPs, high TARDBP expression was corelated with high grade, advanced stage and low macrophage fraction of HCC. We also constructed the hub RBP-circRNA network based on TARDBP and confirmed that hsa_circ_0004913 could bind to TARDBP, which may provide new clues for HCC mechanism study. However, there are also some limitations in our study. First, we only used TCGA, ICGC and CPTAC projects for analysis and little data resulted in only one RBP with prognostic significance, which may lead to the loss of some potential functional RBPs. Second, we didn’t classify samples according to the etiology and these identified circRNAs and RBPs may not be representative in HCC with different etiologies. Moreover, the number of HCC cases with circRNA data included in this study is relatively small. Due to our current lack of HCC samples and no survival information of HCC with circRNA expression profiles in GEO, we could not verify the expression and assess the prognostic value of circRNAs for HCC. In summary, our results indicated that some RBP-circRNA networks take a potential part in the pathogenesis of HCC and provide a new perspective for further mechanism study and biomarker development of HCC."

DOI - https://doi.org/10.18632/aging.203139

Full Text - https://www.aging-us.com/article/203139/text

Correspondence to: Yuhan Chen email: [email protected]

Keywords: hepatocellular carcinoma, autophagy, progression, miR-513b-5p, PIK3R3

Aging-US testimonial from Dr. Kara Fitzgerald ND IFMCP with The Institute for Functional Medicine in Federal Way Washington USA talking about their experience publishing "Potential reversal of epigenetic age using a diet and lifestyle intervention: a pilot randomized clinical trial"

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A groundbreaking clinical trial shows we can reduce biological age (as measured by the Horvath 2013 DNAmAge clock) by more than three years in only eight weeks with diet and lifestyle through balancing DNA methylation.

A first-of-its-kind, peer-reviewed study provides scientific evidence that lifestyle and diet changes can deliver immediate and rapid reduction of our biological age. Since aging is the primary driver of chronic disease, this reduction has the power to help us live better, longer.

The study, released on April 12, utilized a randomized controlled clinical trial conducted among 43 healthy adult males between the ages of 50-72. The 8-week treatment program included diet, sleep, exercise and relaxation guidance, and supplemental probiotics and phytonutrients, resulting in a statistically significant reduction of biological age–over three years younger, compared to controls.

The study was independently conducted by the Helfgott Research Institute, with laboratory assistance from Yale University Center for Genome Analysis, and the results independently analyzed at McGill University and the National University of Natural Medicine.

The study’s lead author, Kara Fitzgerald ND IFMCP, stated that “the combined intervention program was designed to target a specific biological mechanism called DNA methylation, and in particular the DNA methylation patterns that have been identified as highly predictive of biological age. We suspect that this focus was the reason for its remarkable impact. These early results appear to be consistent with, and greatly extend, the very few existing studies that have so far examined the potential for biological age reversal. And it is unique in its use of a safe, non-pharmaceutical dietary and lifestyle program, control group, and the extent of the age reduction. We are currently enrolling participants for a larger study which we expect will corroborate these findings.“

Leading epigeneticist Moshe Szyf PhD of McGill University and co-author on the study adds, “The uniqueness of Dr Fitzgerald approach is that her trial devised a natural but mechanistic driven strategy to target the methylation system of our body. This study provides the first insight into the possibility of using natural alterations to target epigenetic processes and improve our well being and perhaps even longevity and lifespan.”

DNA methylation patterns have become a leading means by which scientists evaluate and track biological aging, a term used to describe the accumulation of damage and loss of function to our cells, tissues and organs. This damage is what drives diseases of aging. “What is extremely exciting,” commented Dr. Fitzgerald, “is that food and lifestyle practices, including specific nutrients and food compounds known to selectively alter DNA methylation, are able to have such an impact on those DNA methylation patterns we know predict aging and age-related disease. I believe that this, together with new possibilities for us all to measure and track our DNA methylation age, will provide significant new opportunities for both scientists and consumers.“

Original Source

https://www.aging-us.com/news_room/three-years-younger-in-just-eight-weeks-a-new-study-suggests-yes

Related Journal Article

http://dx.doi.org/10.18632/aging.202913

Listen to a blog summary of this research paper published by Aging, entitled, "Cdkn1a transcript variant 2 is a marker of aging and cellular senescence."

The phenomenon in which cells are still metabolically active but can no longer proliferate is known as cellular senescence. Cellular senescence is a normal mechanism in development and tissue homeostasis—and a hallmark of aging.

“Most of my lab works on a process called cellular senescence, which is a cellular response to stresses and damage, many of which increase with age,” Dr. Judy Campisi, Professor at the Buck Institute for Research on Aging and Senior Scientist at the Lawrence Berkeley National Lab, said in a recent Aging interview.

An international team of researchers from Dr. Campisi’s lab are in search of new biological markers of cellular senescence and aging. Understanding mechanisms of aging such as senescence is key for developing new, safe interventions that may extend human life—with compounding socioeconomic and cultural impacts. Researchers from this lab come from institutions including the Buck Institute, the University of California, Berkeley’s Lawrence Berkeley National Lab, Universidad de Córdoba, Universidad Mayor, Geroscience Center for Brain Health and Metabolism, and Unity Biotechnology. The team published a trending 2021 paper in Aging‘s Volume 13, Issue 10, entitled, “Cdkn1a transcript variant 2 is a marker of aging and cellular senescence.”

“Our results are, to our knowledge, the first to study Ckdn1a transcript variants in the context of aging.”

There are a number of mechanisms that drive cellular senescence. Previously, mRNA and protein coding gene Cdkn1a transcript variant 1 (p21var1) has been better-studied compared to Cdkn1a transcript variant 2 (p21var2). The authors of this paper explain that this is likely because the encoded protein is identical to that encoded by variant 1, and both variants are regulated by p53. However, neither variants have ever before been studied in the context of aging. In this study, the researchers explored the expression levels of both Cdkn1a transcript variants 1 and 2 in the context of cellular senescence using several tissues from aged mice and a cell culture model of mouse cells.

“The stringent cell growth arrest associated with cellular senescence is determined, among other mechanisms, by activities of cyclin-dependent kinase inhibitor proteins p16Ink4a and p21Cip1/Waf1, encoded by the Cdkn2a and Cdkn1a loci, respectively [1].”

Study results showed that both variants are induced during cellular senescence. They showed that p21var1 and p21var2 are equally sensitive to transcriptional upregulation after p53 stabilization. The in vitro models also found that p21var2 is preferentially induced with age.

“In sum, p21var2 expression is consistently elevated with age, in contrast with an absence of age-related change in p21var1 levels.”

The researchers conducted further tests in vivo to examine the expression pattern of p21var2 and their results suggested that the circadian regulation of p21Cip1/Waf1 is driven solely by expression of Cdkn1a transcript variant 1. The team also induced cellular senescence in vivo with doxorubicin and ABT-263 (navitoclax) and evaluated the variants’ expression. These results confirmed their in vitro findings that p21var2 is more prone to cellular senescence than p21var1, thus making it a better marker for assessing the presence of senescent cells in vivo.

“We show that, although tissue-specific exceptions may arise, p21var2 but not p21var1 is a better candidate marker of aging and senescence in mice.”

DOI - doi.org/10.18632/aging.203110

Full Text - www.aging-us.com/article/203110/text

Correspondence to: Judith Campisi email: [email protected]

About Aging

Please visit our website at www.Aging-US.com​​

Aging is published by Impact Journals, LLC please visit www.ImpactJournals.com​​ or connect with @ImpactJrnls

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Aging published "Cdkn1a transcript variant 2 is a marker of aging and cellular senescence" which reported that cellular senescence is a cell fate response characterized by a permanent cell cycle arrest driven primarily the by cell cycle inhibitor and tumor suppressor proteins p16Ink4a and p21Cip1/Waf1. In mice, the p21Cip1/Waf1 encoding locus, Cdkn1a, is known to generate two transcripts that produce identical proteins, but one of these transcript variants is poorly characterized.

The authors show that the Cdkn1a transcript variant 2, but not the better-studied variant 1, is selectively elevated during natural aging across multiple mouse tissues.

Importantly, mouse cells induced to senescence in culture by genotoxic stress upregulated both transcripts, but with different temporal dynamics: variant 1 responded nearly immediately to genotoxic stress, whereas variant 2 increased much more slowly as cells acquired senescent characteristics.

Upon treating mice systemically with doxorubicin, which induces widespread cellular senescence in vivo, variant 2 increased to a larger extent than variant 1. Variant 2 levels were also more sensitive to the senolytic drug ABT-263 in naturally aged mice.

Thus, variant 2 is a novel and more sensitive marker than variant 1 or total p21Cip1/Waf1 protein for assessing the senescent cell burden and clearance in mice.

Dr. Judith Campisi from The Buck Institute for Research on Aging as well as The University of California said, "The stringent cell growth arrest associated with cellular senescence is determined, among other mechanisms, by activities of cyclin-dependent kinase inhibitor proteins p16Ink4a and p21Cip1/Waf1, encoded by the Cdkn2a and Cdkn1a loci, respectively."

The increased expression of these proteins is a major hallmark of senescence in most cells, and therefore have become markers of senescence both in culture and in vivo.

Consistent with the fact that senescent cells increase with age in many mouse and human tissues, Cdkn2a mRNA levels also increase with age in these tissues.

To date, possible changes in the expression of Cdkn1a transcript-specific variants during age or cellular senescence have not been explored.

The authors also analyze expression levels in a cell culture model of mouse cells subjected to genotoxic stress-induced senescence to evaluate their relative utility as senescence markers both in culture and in vivo.

The Campisi Research Team concluded in their Aging Research Output that it remains unexplored the possibility that the different transcript variants are preferentially associated with one or other cell fate.

Human cells also express several Cdkn1a transcript variants.

Among the ten human transcript variants currently annotated, at least one shares translational regulatory mechanisms with the murine p21var2.

Interestingly, even though murine variant 2 and human variant 4 do not appear to share sequence homology, the translational regulation in both transcripts is driven by the integrated stress response and results in cell cycle arrest.

The potential relevance of this mechanism for cellular senescence in humans remains unknown, and the functions and interrelations of the different Cdkn1a transcript variants have not been studied in depth.

DOI - https://doi.org/10.18632/aging.203110

Full Text - https://www.aging-us.com/article/203110/text

Correspondence to: Judith Campisi email: [email protected]

Keywords: p21, p53, mouse dermal fibroblast, ionizing radiation, doxorubicin

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.

In 2021, researchers from Harvard University and the Broad Institute wrote a theory article that was published in Aging’s Volume 13, Issue 12, and entitled, “Shifting epigenetic contexts influence regulatory variation and disease risk.” The authors described common epigenetic trends throughout human growth, development, and aging. They also aimed to show how changing epigenetic contexts may influence the behavior of evolutionary forces and risk of genetic disease.

FETAL TO ADULT EPIGENETIC SHIFTS

The researchers point out that in order to better understand the contribution of epigenetic changes to disease and aging, it is important to understand the developmental changes that occur between fetal and adult tissues, and their interaction with epigenetic aging.

“Furthermore, these fetal to adult epigenetic shifts can be compounded by additional modifications through aging-associated epigenetic changes.”

Characterizing these epigenetic trends and examining their potential interaction with later-in-life epigenetic aging were main goals of this study. In order to do this, the researchers defined genomic regions where, over the course of development and aging, chromatin accessibility consistently shifts. Chromatin can be broadly classified in either of two epigenetic states: activating or repressing modifications. These states refer to chromatin accessibility and the increased or decreased ability of DNA to access gene-regulatory machinery, such as transcription factors. The authors note that they used an accessibility-based definition of epigenetic context, and that there are other marks of epigenetic changes (e.g. methylation, and etc.) that are not captured by this definition.

“Epigenetic marks established during development can persist into adulthood, but they do so in the context of shifts in epigenetic states as tissues transition into their adult forms and functions.”

Read the full blog post: https://www.impactjournals.com/journals/blog/aging/trending-with-impact-epigenetic-shifts-aging-and-disease/

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DOI - https://doi.org/10.18632/aging.203194

Full text - https://www.aging-us.com/article/203194/text

Correspondence to: Terence D. Capellini email: [email protected]

Keywords: development, evolution, GWAS, disease, aging

About Aging

Launched in 2009, Aging 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 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.

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Aging published this theory article on November 17, 2018, entitled, “Disease or not, aging is easily treatable,” by Dr. Mikhail V. Blagosklonny from the Department of Cell Stress Biology, Roswell Park Comprehensive Cancer Center, Buffalo, NY.

Abstract:

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.

To date, this study has generated an Altmetric Attention Score of 54. The Altmetric Attention Score provides an at-a-glance indication of the volume and type of online attention the research has received.

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DOI - https://doi.org/10.18632/aging.101647

Full text - https://www.aging-us.com/article/101647/text

Correspondence to: Mikhail V. Blagosklonny email: [email protected]

Keywords: gerossuppresants, senolytics, longevity, lifespan, aging

About Aging

Launched in 2009, Aging 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 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 on:

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Our bodies are quite miraculous machines. We are born with a genome that contains the code for every protein necessary for survival. We develop and produce hormones that allow us to reproduce and have children. But what happens to us as we age? This question has puzzled scientists for years while they offer theory after theory.

In 1957, evolutionary biologist George Williams proposed what he called the antagonistic pleiotropy hypothesis as a theory of how and why we age. He claimed that our bodies express a gene that has benefits for our early life, but that same gene will harm us later on. His hypothesis has inspired aging research and led to a story about a chemical discovered deep within the dirt of an island floating in the Pacific.

In 1964, Canadian researchers, led by Stanley Skoryna from McGill University, set sail out of Halifax for Easter Island—a speck of land floating 2,000 miles off the coast of Chile, where the human population is small but life is diverse. They were hoping to retrieve precious specimens from the island before its land was tarnished with the building of a new airport. Stanley and his team collected hundreds of plant samples, countless animal specimens, and took blood and saliva from all 949 of the island’s residents.

What they found buried in the dirt on Easter Island would turn out to be the biggest treasure of all: a bacteria that would mystify scientists for the next 50 years. This bacteria was found to create a chemical now known as rapamycin, cleverly named after Easter Island’s native name, Rapa Nui.

Read the full article: https://www.impactjournals.com/journals/blog/aging/rapamycin-miracle-chemical-discovered-easter-islands-dirt/

About Aging

Launched in 2009, Aging 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 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 on:

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Aging published "Potential reversal of epigenetic age using a diet and lifestyle intervention: a pilot randomized clinical trial" which reported on a randomized controlled clinical trial conducted among 43 healthy adult males between the ages of 50-72. The 8-week treatment program included diet, sleep, exercise and relaxation guidance, and supplemental probiotics and phytonutrients.

Genome-wide DNA methylation analysis was conducted on saliva samples using the Illumina Methylation Epic Array and DNAmAge was calculated using the online Horvath DNAmAge clock (also published in Aging).

The diet and lifestyle treatment was associated with a 3.23 years decrease in DNAmAge compared with controls.

DNAmAge of those in the treatment group decreased by an average 1.96 years by the end of the program compared to the same individuals at the beginning with a strong trend towards significance.

This randomized controlled study, published in Aging, suggests that specific diet and lifestyle interventions may reverse Horvath DNAmAge epigenetic aging in healthy adult males.

The study’s lead author, Kara Fitzgerald ND IFMCP, from The Institute for Functional Medicine said, "Advanced age is the largest risk factor for impaired mental and physical function and many non-communicable diseases including cancer, neurodegeneration, type 2 diabetes, and cardiovascular disease."

Methylation clocks are based on systematic methylation changes with age.

DNAmAge clock specifically demonstrates about 60% of CpG sites losing methylation with age and 40% gaining methylation.

Almost a quarter of the DNAmAge CpG sites are located in glucocorticoid response elements, pointing to a likely relationship between stress and accelerated aging. Cumulative lifetime stress has been shown to be associated with accelerated aging of the methylome.

Other findings include that PTSD contributes to accelerated methylation age; and that greater infant distress is associated with an underdeveloped, younger epigenetic age.

This is to say the authors have tentatively accepted the hypothesis that the methylation pattern from which the DNAmAge clock is computed is a driver of aging, thus they expect that attempting to directly influence the DNA methylome using diet and lifestyle to set back DNAmAge will lead to a healthier, more “youthful” metabolism.

The Fitzgerald Research Team concluded in their Aging Research Output, "it may be that emerging ‘omics’ approaches continue to evolve our understanding of biological age prediction and reversal beyond DNA methylation alone. Integration of our future understanding of multi-omics data should therefore be considered in the future trials of candidate age-delaying interventions."

DOI - https://doi.org/10.18632/aging.202913

Full Text - https://www.aging-us.com/article/202913/text

Correspondence to: Kara N. Fitzgerald email: [email protected]

Keywords: DNA methylation, epigenetic, aging, lifestyle, biological clock

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.

To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl

Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls

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Aging published this research paper on March 14, 2021, entitled, “Deep longitudinal phenotyping of wearable sensor data reveals independent markers of longevity, stress, and resilience,” by researchers from Gero PTE. LTD., Singapore 409051, Singapore and Moscow Institute of Physics and Technology, Moscow Region 141700, Russia.

Abstract:

Biological age acceleration (BAA) models based on blood tests or DNA methylation emerge as a de facto standard for quantitative characterizations of the aging process. We demonstrate that deep neural networks trained to predict morbidity risk from wearable sensor data can provide a high-quality and cheap alternative for BAA determination. The GeroSense BAA model was trained and validated using steps per minute recordings from 103,830 one-week long and 2,599 of up to 2 years-long longitudinal samples and exhibited a superior association with life-expectancy over the average number of steps per day in, e.g., groups stratified by professional occupations. The association between the BAA and effects of lifestyles, the prevalence of future incidence of diseases was comparable to that of BAA from models based on blood test results. Wearable sensors let sampling of BAA fluctuations at time scales corresponding to days and weeks and revealed the divergence of organism state recovery time (resilience) as a function of chronological age. The number of individuals suffering from the lack of resilience increased exponentially with age at a rate compatible with Gompertz mortality law. We speculate that due to the stochastic character of BAA fluctuations, its mean and auto-correlation properties together comprise the minimum set of biomarkers of aging in humans.

To date, this study has generated an Altmetric Attention Score of 43. The Altmetric Attention Score provides an at-a-glance indication of the volume and type of online attention the research has received.

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DOI - https://doi.org/10.18632/aging.202816

Full text - https://www.aging-us.com/article/202816/text

Correspondence to: Timothy V. Pyrkov email: [email protected] and Peter O. Fedichev email: [email protected]

Keywords: biological age acceleration (BAA), public health, personalized interventions, Gompertz law, resilience, aging

About Aging

Launched in 2009, Aging 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 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 on:

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Aging published this trending editorial on May 20, 2021, entitled, “When aging switches on Alzheimer’s” by researchers from the Department of Biomedical Engineering, MIND Institute, Center for Neurobiology of Learning and Memory, University of California, Irvine, CA.

In the paper, the researchers discuss the effects of oxidative stress in aging and Alzheimer’s disease. In short, age-related oxidative stress launches a global shift in the epigenetic landscape, and drives metabolic and energetic “switches.” The researchers point out that these "switches" highlight potential epigenetic targets for the treatment of Alzheimer’s disease.

To date, this study has generated an Altmetric Attention Score of 22. The Altmetric Attention Score provides an at-a-glance indication of the volume and type of online attention the research has received.

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DOI - https://doi.org/10.18632/aging.203085

Full text - https://www.aging-us.com/article/203085/pdf (PDF Download)

Correspondence to: Gregory J. Brewer email: [email protected]

Keywords: Alzheimer’s disease, NAD+/NADH, oxidative shift, mitochondrial impairment, neuroinflammation, aging

About Aging

Launched in 2009, Aging 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 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 on:

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Aging is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

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