Aging-US

Aging-US Podcast

Aging-US is dedicated to advancing our understanding of the biological mechanisms that drive aging and the development of age-related diseases. Our mission is to serve as a platform for high-quality research that uncovers the cellular, molecular, and systemic processes underlying aging, and translates these insights into strategies to extend healthspan and delay the onset of chronic disease. Read about the Aging-US Scientific Integrity Process: https://aging-us.com/scientific-integrity

  1. Human Telomerase Shows Selective Cross-Species Activity, Revealing Limits of Animal Models

    1D AGO

    Human Telomerase Shows Selective Cross-Species Activity, Revealing Limits of Animal Models

    BUFFALO, NY — May 5, 2026 — A new #research paper was #published in Volume 18 of Aging-US on April 13, 2026, titled “Cross species activity of TERT human telomerase component.” The study was led by co–first authors Raúl Sánchez-Vázquez and Paula Martínez, with María A. Blasco serving as corresponding author, from the Spanish National Cancer Centre (CNIO), Madrid, Spain. In this study, the researchers explored a key question in aging and regenerative medicine: can the human telomerase protein function effectively in other species commonly used in preclinical research? Telomerase plays a central role in maintaining chromosome integrity by preventing telomere shortening—a process closely linked to cellular aging and disease. To investigate this, the team introduced the human telomerase catalytic subunit (TERT) into primary lung fibroblasts from several mammalian species, including monkey, pig, rabbit, rat, dog, and mouse. They then assessed both biochemical activity and the ability of telomerase to extend telomeres over time. The results revealed a clear distinction between biochemical compatibility and true biological function. In vitro, human TERT was able to form active complexes with telomerase RNA from several species, including monkey, pig, rabbit, and rat. However, this activity did not always translate into effective telomere maintenance in living cells. Notably, only human and non-human primate cells showed progressive telomere lengthening over time. In contrast, other species—even those showing initial enzymatic activity—failed to sustain telomere extension during long-term culture. In some cases, telomeres continued to shorten, suggesting that functional integration of telomerase depends on additional species-specific factors. The study also uncovered important limitations in commonly used animal models. Mouse and canine cells did not support human TERT activity, and in some cases, expression of the human enzyme led to reduced cell viability and signs of cellular stress. “These results reveal that only non-human primate cells support full functional activity of the human telomerase protein in a cellular context, underscoring their suitability as preclinical models for telomerase-based therapeutic strategies.” Importantly, the findings highlight that successful telomerase activity in a test tube does not necessarily reflect what happens inside a living cell. The recruitment, regulation, and function of telomerase depend on a complex network of interacting proteins and cellular processes, many of which differ across species. Overall, this study provides important insight into the challenges of translating telomerase-based therapies from preclinical models to humans. By identifying non-human primates as the most compatible system, the work offers a clearer path forward for developing therapies aimed at treating telomere-related diseases and age-associated conditions. DOI - https://doi.org/10.18632/aging.206372 Corresponding author - Maria A. Blasco - mblasco@cnio.es Abstract video - https://www.youtube.com/watch?v=XxjjId5i_Ww Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, telomeres, telomerase To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    4 min
  2. Aging-US Supports the NOVA Conference 2026

    6D AGO

    Aging-US Supports the NOVA Conference 2026

    On April 25, 2026, the NOVA (Neuroscience of Vitality and Aging) Conference brought together a dynamic and interdisciplinary audience in Boston, MA. With over 600 attendees spanning students, researchers, clinicians, investors, and patient advocates, the event highlighted both the complexity of brain aging and the growing momentum behind efforts to better understand and treat neurodegenerative diseases. In the opening keynote, Dr. Joanne Smikle of the American Brain Foundation emphasized the need to remember the “why” behind this research. She highlighted the power of intentional collaboration and the belief that breakthroughs in one neurological disease may translate to others. Even small monthly contributions as little as $10.00 can collectively drive meaningful progress. Full recap - https://aging-us.org/2026/04/aging-us-supports-the-nova-conference-2026/ Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    9 min
  3. Stage-Specific Gene Expression Changes Reveal Early Triggers of Cellular Aging

    APR 29

    Stage-Specific Gene Expression Changes Reveal Early Triggers of Cellular Aging

    BUFFALO, NY — April 29, 2026 — A new #research paper was #published in Volume 18 of Aging-US on April 10, 2026, titled “Stage-dependent transcriptomic changes in human dermal fibroblast senescence model.” The study was led by first author Michiko Kudo from the University of Tokyo and DHC Corporation Laboratories and corresponding author Shuichi Asakawa from the University of Tokyo. In this work, the researchers took a closer look at how gene expression changes as cells age, focusing on human dermal fibroblasts—a widely used model for studying aging in skin and connective tissues. While cellular senescence is known to play a central role in aging, the timing and progression of molecular changes during this process have remained difficult to define. To explore this, the team developed a stepwise model of replicative senescence, categorizing cells into three stages—young, middle, and old—based on their cumulative number of divisions. This approach allowed them to capture the gradual nature of aging, rather than relying on acute stress models that may overlook early-stage transitions. One of the more interesting findings was that the “middle” stage—often overlooked—is not just a simple midpoint, but a biologically active transition phase. Although gene expression profiles in young and middle cells appeared similar at first glance, a closer look showed that important molecular changes had already begun during this phase. In particular, genes involved in immune and inflammatory responses were activated early, even before cells reached full senescence. This suggests that aging-related inflammation may begin much earlier than previously appreciated, gradually intensifying as cells progress toward the late stage. At the same time, genes responsible for maintaining basic cellular functions—such as protein synthesis, cell structure, and adhesion—showed a progressive decline as aging advanced. Together, these changes suggest a shift in cellular priorities, where stress and inflammatory signals increase while maintenance and repair functions gradually decline. To better understand these patterns, the researchers combined transcriptomic analysis with network and matrix factorization approaches. These methods revealed distinct gene expression programs associated with different stages of aging, including early immune activation, mid-stage extracellular remodeling, and late-stage functional decline. “These findings suggest that immune–inflammatory responses are engaged from early senescence, whereas cell adhesion and maintenance pathways decline progressively.” Importantly, the results point to the middle stage of senescence as a potential window for intervention. Unlike fully senescent cells, which exhibit more stable and potentially irreversible changes, cells in this transitional phase may retain some degree of plasticity, making them more responsive to therapeutic strategies. Overall, this study offers a clearer picture of how aging unfolds at the molecular level. By identifying stage-specific changes in gene expression, the authors provide new insight into the early drivers of cellular senescence and highlight potential targets for delaying or modifying age-related decline. DOI - https://doi.org/10.18632/aging.206371 Corresponding author - Shuichi Asakawa - asakawa@g.ecc.u-tokyo.ac.jp Abstract video - https://www.youtube.com/watch?v=DZNfYmj4DW8 Website - https://www.Aging-US.com​​ Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    4 min
  4. P38 MAPK–Driven Epigenetic Regulation Identified as a Key Mechanism in Lung Fibrosis

    APR 27

    P38 MAPK–Driven Epigenetic Regulation Identified as a Key Mechanism in Lung Fibrosis

    Aging has long been linked to a range of biological processes, including cellular senescence, epigenetic changes, and chronic tissue remodeling. Yet, these explanations often describe what happens during aging rather than why certain age-related diseases, such as fibrosis, continue to progress over time. In conditions like idiopathic pulmonary fibrosis (IPF), a key question remains: what drives the persistent activation of cells that should normally return to a resting state after injury? Increasing attention has turned to the interaction between cellular signaling pathways and epigenetic regulation as a potential explanation. Understanding how these processes work together to control gene expression and cell behavior is becoming an important focus in uncovering the mechanisms behind age-related disease. A new research paper was published in Volume 18 of Aging-US, titled “P38 MAPK is involved in epigenetic regulation of fibrotic genes in replication induced senescence in lung fibroblasts.” The study was led by first author Shan Zhu and corresponding author Yan Y. Sanders from the Department of Biomedical and Translational Sciences, Eastern Virginia Medical School (Macon & Joan Brock Virginia Health Sciences at Old Dominion University), in collaboration with Jennifer Q. Zhou, Kan Wang, and Ming-lei Guo from the same institution. Full blog - https://aging-us.org/2026/04/p38-mapk-driven-epigenetic-regulation-identified-as-a-key-mechanism-in-lung-fibrosis/ Paper DOI - https://doi.org/10.18632/aging.206357 Corresponding author - Yan Y Sanders - sandery@odu.edu Abstract video - https://www.youtube.com/watch?v=yP0CwWMUhnY Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206357 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senescence, fibroblast activation, p38 MAPK, lung fibrosis, H4K16Ac To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    6 min
  5. From Hydra to Rotifers: A New Hypothesis Explores Pathways to Delay Aging in Humans

    APR 27

    From Hydra to Rotifers: A New Hypothesis Explores Pathways to Delay Aging in Humans

    BUFFALO, NY — April 27, 2026 — A new #hypothesis paper was #published in Volume 18 of Aging-US on April 8, 2026, titled “From Hydra to rotifer and beyond: implications for human aging and delayed senescence.” The study was led by first and corresponding author Michael Bordonaro from the Geisinger College of Health Sciences. In this work, the author explores a bold and testable hypothesis centered on two very different invertebrate models of aging: the freshwater cnidarian Hydra and the rotifer Brachionus manjavacas. Hydra are well known for their remarkable ability to maintain tissue integrity over time through continuous stem cell renewal, effectively avoiding many of the hallmarks of aging under laboratory conditions. In contrast, rotifers represent the opposite end of the biological spectrum, with short lifespans, fixed somatic cell numbers, and a predictable pattern of age-related decline. Building on these contrasts, the paper proposes that introducing Hydra-like gene expression patterns into rotifers could delay senescence and extend healthspan. The hypothesis focuses in particular on conserved molecular pathways, including the transcription factor FoxO, which plays a central role in maintaining stem cell function and cellular resilience. Rather than attempting to recreate full stem cell renewal in rotifers—an organism with a fixed adult cell number—the proposed strategy emphasizes improving cellular maintenance, stress resistance, and proteostasis within existing cells. The paper outlines an iterative experimental framework, beginning with targeted genetic manipulation in rotifers and extending to more complex organisms such as Daphnia and mouse models. This stepwise approach is designed to identify which elements of the Hydra genetic program are truly responsible for its resistance to aging, while also allowing researchers to monitor potential trade-offs, including increased risk of uncontrolled cell growth. “We hypothesize that delayed senescence at the organismal level is possible through recapitulation of Hydra-like patterns of gene expression in rotifers, and that data obtained may help generate hypotheses for somatic interventions and prioritize pathways for mammalian validation in future studies.” Importantly, the author emphasizes that complete elimination of aging is unlikely in complex organisms due to evolutionary and biological constraints. Instead, the goal is more realistic: extending healthspan and delaying the onset of age-related decline. The paper also highlights the importance of balancing potential benefits with risks, particularly the possibility that enhancing cellular renewal pathways could increase susceptibility to neoplasia. Overall, this study presents a conceptual and experimental roadmap for translating insights from simple organisms into strategies that may eventually inform human aging research. By bridging the gap between negligible senescence and rapid aging models, the work provides a fresh perspective on how conserved biological mechanisms might be harnessed to improve health across the lifespan. DOI - https://doi.org/10.18632/aging.206370 Corresponding author - Michael Bordonaro - mbordonaro1@geisinger.edu Abstract video - https://www.youtube.com/watch?v=YGzYf3W5jNA To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    4 min
  6. Epigenetic Aging Linked to MRI Signatures of Neurodegeneration but Not General Brain Aging

    APR 23

    Epigenetic Aging Linked to MRI Signatures of Neurodegeneration but Not General Brain Aging

    BUFFALO, NY — April 23, 2026 — A new #research paper was #published in Volume 18 of Aging-US on April 7, 2026, titled “Association of epigenetic age acceleration with MRI biomarkers of aging and Alzheimer’s disease neurodegeneration.” The study was led by first and corresponding author Linda K. McEvoy from the Kaiser Permanente Washington Health Research Institute, in collaboration with a multidisciplinary team of researchers across leading institutions in the United States and Europe. In this study, the researchers examined whether epigenetic measures of biological aging are associated with structural brain changes linked to aging and Alzheimer’s disease. Using data from 1,196 older women enrolled in the Women’s Health Initiative Memory Study, they analyzed five widely used epigenetic clocks and compared them with MRI-derived measures obtained approximately eight years later. The findings revealed a clear distinction between different aspects of aging. None of the epigenetic clocks were associated with accelerated brain aging as measured by the SPARE-BA index, a composite MRI marker of brain age. However, one specific clock—AgeAccelGrim2—was significantly associated with the Alzheimer’s Disease Pattern Similarity Score (AD-PS), a validated imaging biomarker linked to increased risk of dementia. Further analyses suggested that this association was largely driven by epigenetic signatures related to smoking exposure. In particular, a DNA methylation marker reflecting cumulative smoking history was linked to reduced frontal and temporal lobe volumes—regions commonly affected in age-related neurodegeneration. Notably, no significant associations were observed with hippocampal or entorhinal cortex volumes, areas more directly implicated in early Alzheimer’s pathology. “Taken together with prior findings, these results suggest that measures of epigenetic and brain age acceleration capture different aspects of biological aging, and that AgeAccelGrim2 is predictive of neurodegenerative changes associated with smoking that increase risk of dementia.” The study highlights the complexity of biological aging and underscores that not all aging biomarkers reflect the same underlying processes. While epigenetic clocks are increasingly used to estimate biological age, their relationship with brain structure appears to depend on the specific pathways they capture—particularly those influenced by environmental exposures such as smoking. Overall, these findings provide important insight into how molecular measures of aging relate to neuroimaging markers of brain health. By distinguishing between general brain aging and disease-related neurodegeneration, this work helps refine the use of epigenetic biomarkers in aging research and may support future efforts to identify individuals at risk for cognitive decline. DOI - https://doi.org/10.18632/aging.206369 Corresponding author - Linda K. McEvoy - linda.k.mcevoy@kp.org Abstract video - https://www.youtube.com/watch?v=kZiRjlKnnsI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206369 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, epigenetic clocks, brain age, biological aging, smoking, frontal lobe To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    3 min
  7. Global Experts Highlight Path Toward Actionable Interventions in Human Aging

    APR 21

    Global Experts Highlight Path Toward Actionable Interventions in Human Aging

    BUFFALO, NY — April 21, 2026 — A new meeting report was published in Volume 18 of Aging-US on April 6, 2026, titled “Toward actionable interventions in human aging (12th ARDD meeting, 2025).” The report was led by corresponding authors Aleksandr Dekan and Daniela Bakula from the University of Copenhagen, Denmark, in collaboration with an international group of researchers spanning academia, industry, and biotechnology. Bringing together experts from across the global aging research community, the 12th ARDD meeting focused on one central goal: moving beyond descriptive studies of aging toward interventions that can actively improve human healthspan. The discussions reflected a clear shift in the field—from understanding the hallmarks of aging to identifying the molecular mechanisms that can be targeted to modify them. Key presentations explored whether biological age can be reversed, highlighting the epigenome as a central regulator of cellular identity. Emerging evidence suggests that partial cellular reprogramming may restore youthful function, while systemic effects observed in preclinical models point to the possibility of organ-wide or even whole-body rejuvenation. The meeting also emphasized the importance of maintaining genomic integrity, with accumulating DNA damage linked to widespread transcriptional stress and age-associated functional decline. At the same time, chronic inflammation, metabolic dysfunction, and cellular senescence were consistently identified as major drivers of aging, reinforcing the need for integrated, multi-targeted therapeutic strategies. Advances in biomarker development were another major focus. Researchers presented new generations of biological aging clocks—ranging from organ-specific proteomic signatures to single-cell and imaging-based approaches—capable of predicting disease risk and monitoring intervention outcomes with increasing precision. In parallel, the integration of artificial intelligence into drug discovery is accelerating the development of novel therapeutics. From generative AI-designed proteins to platform-based identification of new drug targets, these approaches are helping bridge the gap between basic research and clinical application. “This focus is predicated on the hypothesis that aging is not solely a result of stochastic damage accumulation but may be a tractable, modifiable, and potentially reversible biological process amenable to intervention.” Beyond laboratory science, the meeting highlighted the growing importance of translational strategies, regulatory pathways, and investment models in bringing anti-aging therapies to market. A consensus emerged around a “disease-first” approach, in which targeting specific age-related conditions may provide a practical pathway for validating interventions that also influence underlying aging biology. Overall, the ARDD 2025 meeting underscored a major turning point in the field. Aging research is no longer confined to observation—it is increasingly positioned to deliver actionable interventions that could reshape how age-related diseases are prevented and treated. DOI - https://doi.org/10.18632/aging.206368 Corresponding authors - Aleksandr Dekan - adekan@sund.ku.dk, and Daniela Bakula - bakula@sund.ku.dk Video abstract - https://www.youtube.com/watch?v=LntAWVQMKqE To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    4 min
  8. Modeling Premature Aging in Yeast Reveals Key Effects of Progerin on Cellular Lifespan

    APR 17

    Modeling Premature Aging in Yeast Reveals Key Effects of Progerin on Cellular Lifespan

    BUFFALO, NY — April 17, 2026 — A new #research paper was #published in Volume 18 of Aging-US on April 3, 2026, titled “Modeling premature aging in yeast via the expression of Progerin.” The study was led by first author Zachery R. Belak from the University of Saskatchewan, and corresponding author Troy A.A. Harkness from the University of Saskatchewan and the University of Alberta. The team developed a yeast-based model to study premature aging by expressing Progerin, the toxic protein responsible for Hutchinson–Gilford Progeria Syndrome. Using genetically engineered yeast cells, they compared the effects of Progerin with its normal counterpart, Lamin A, to better understand how protein accumulation impacts cellular aging. Their findings show that Progerin expression leads to slower cell growth, increased genome instability, and a significant reduction in chronological lifespan. In contrast, Lamin A did not produce the same harmful effects, highlighting the specific role of Progerin in driving premature aging phenotypes. The study also demonstrates that Progerin accumulates in aging mother cells and remains more stable than Lamin A, suggesting a mechanism by which damaged or toxic proteins are retained during the aging process. These observations mirror what has been reported in human cells, reinforcing the relevance of this model system. “Taken together, expression of Progerin in yeast cells mimics what is observed in human cells, establishing yeast as a powerful model to discover genetic mechanisms driving premature and normal aging.” Overall, the researchers present a practical and efficient model for studying the biological mechanisms underlying premature aging. Their work provides a valuable platform for testing new strategies aimed at reducing toxic protein accumulation and improving cellular health during aging. DOI - https://doi.org/10.18632/aging.206367 Corresponding author - Troy AA. Harkness - taharkne@ualberta.ca Abstract video - https://www.youtube.com/watch?v=VYQKAJjgIb8 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206367 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Hutchinson-Gilford Progeria Syndrome, yeast, Progerin, Lamin A, premature aging To learn more about the journal, please visit https://www.Aging-US.com​​ and connect with us on social media at: Bluesky - https://bsky.app/profile/aging-us.bsky.social ResearchGate - https://www.researchgate.net/journal/Aging-1945-4589 X - https://twitter.com/AgingJrnl Facebook - https://www.facebook.com/AgingUS/ Instagram - https://www.instagram.com/agingjrnl/ LinkedIn - https://www.linkedin.com/company/aging/ Reddit - https://www.reddit.com/user/AgingUS/ Pinterest - https://www.pinterest.com/AgingUS/ YouTube - https://www.youtube.com/@Aging-US Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

    3 min

Ratings & Reviews

4
out of 5
2 Ratings

About

Aging-US is dedicated to advancing our understanding of the biological mechanisms that drive aging and the development of age-related diseases. Our mission is to serve as a platform for high-quality research that uncovers the cellular, molecular, and systemic processes underlying aging, and translates these insights into strategies to extend healthspan and delay the onset of chronic disease. Read about the Aging-US Scientific Integrity Process: https://aging-us.com/scientific-integrity

You Might Also Like