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Aging-US

Aging-US

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 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-integrityAll rights reserved Wissenschaft
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  • New Single-Cell Transcriptomic Clock Reveals Intrinsic and Systemic T Cell Aging in COVID-19 and HIV

    New Single-Cell Transcriptomic Clock Reveals Intrinsic and Systemic T Cell Aging in COVID-19 and HIV
    Feb 19 2026
    BUFFALO, NY — February 19, 2026 — A new #research paper was #published in Volume 18 of Aging-US on February 8, 2026, titled “Single-cell transcriptomics reveal intrinsic and systemic T cell aging in COVID-19 and HIV.” In this study, co-first authors Alan Tomusiak from the Buck Institute for Research on Aging and the University of Southern California, and Sierra Lore from the Buck Institute for Research on Aging and the University of Copenhagen, together with corresponding author Eric Verdin from the Buck Institute for Research on Aging, developed a new single-cell transcriptomic clock called T immune cell transcriptomic clock (Tictock) to measure aging in specific immune cells. Immune aging increases susceptibility to infection, cancer, and chronic inflammatory disease. Most aging clocks, used to measure it, rely on bulk measurements from mixed cell populations. As a result, they cannot determine whether age-related signals reflect shifts in cell proportions or true molecular aging within defined immune cells. To address this limitation, the research team used single-cell RNA sequencing, a method that measures gene expression in individual cells. They analyzed nearly two million immune cells from the blood of healthy adults to develop Tictock. This tool integrates automated classification of six canonical T cell subsets with cell-type specific age prediction models. This design enables the separation of systemic aging, reflected by changes in cell proportions, from intrinsic aging, which occurs within individual cells. When the team applied Tictock to patients with acute COVID-19, they found two clear effects. First, COVID-19 altered T cell composition, including significant reductions in naïve CD8 and naïve CD4 T cells. Second, the infection increased the biological age of naïve CD8 T cells. In people living with HIV who were receiving long-term antiretroviral therapy, T cell proportions remained largely stable. However, naïve CD8 T cells still showed signs of accelerated aging. The study also uncovered shared biological pathways linked to immune aging. Many of the genes that predicted age were involved in ribosomes, the structures that help cells produce proteins. The researchers also observed that older immune cells often had shorter average transcript lengths, a feature previously linked to aging. These findings suggest that changes in protein production and gene regulation play an important role in immune decline. “Gene Ontology enrichment of 209 genes shared across six clock models identified common pathways including the cytosolic small ribosomal subunit, TNF receptor binding, and cytosolic ribosome components.” Overall, Tictock was designed to measure relative aging within defined T cell populations rather than overall biological aging. By distinguishing systemic from cell-intrinsic immune aging, it provides a clearer understanding of how viral infections such as COVID-19 and HIV reshape immune function. This approach enables the study of immune aging at single-cell resolution and may support improved immune risk assessment in clinical and research settings. DOI - https://doi.org/10.18632/aging.206353 Corresponding author - Eric Verdin - EVerdin@buckinstitute.org Abstract video - https://www.youtube.com/watch?v=_r3AF7OrgKY 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​​. MEDIA@IMPACTJOURNALS.COM
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    4 Min.
  • Polyploidy-Induced Senescence May Drive Aging, Tissue Repair, and Cancer Risk

    Polyploidy-Induced Senescence May Drive Aging, Tissue Repair, and Cancer Risk
    Feb 18 2026
    BUFFALO, NY — February 18, 2026 — A new #editorial was #published in Volume 18 of Aging-US on February 8, 2026, titled “Polyploidy-induced senescence: Linking development, differentiation, repair, and (possibly) cancer?” In this editorial, Iman M. Al-Naggar of the University of Connecticut School of Medicine, UConn Health, and the University of Connecticut Center on Aging, with George A. Kuchel of the University of Connecticut Center on Aging, examines the biological and clinical significance of polyploidy-induced senescence. The authors discuss how this process may contribute to normal tissue development and long-term repair, while also influencing cancer risk. Their perspective centers on the bladder and outlines how aging-related cellular changes may shape tumor initiation. Aging remains the strongest risk factor for bladder cancer, which is predominantly of urothelial origin. Cellular senescence is defined as a stable growth arrest in which cells remain metabolically active but no longer divide. Polyploidy refers to cells that contain extra copies of their genome. Although polyploidy is frequently associated with cancer, it also occurs in several healthy tissues as part of normal development and adaptation to stress. The editorial highlights increasing evidence that polyploidy and senescence can function together as a coordinated biological program. The authors focus on bladder umbrella cells, which form the barrier between urine and the bloodstream. In mice, these cells naturally become polyploid early in life and display markers of senescence across the lifespan. Rather than representing dysfunction, this state may help maintain tissue architecture, reinforce barrier integrity, and support resistance to environmental stress. In this context, polyploidy-induced senescence may act as a differentiation program that preserves organ structure. “Polyploidization and senescence may be interrelated stress responses, yet they have been studied mostly in isolation.” However, this protective mechanism may become unstable. Polyploidy-induced senescence depends on intact tumor suppressor pathways, including regulators such as p16. If these safeguards are lost through mutation, deletion, or epigenetic silencing, polyploid senescent cells may escape growth arrest. Re-entry into the cell cycle under these conditions may promote chromosomal instability and aneuploidy, increasing the likelihood of malignant transformation. The authors propose that a subset of bladder cancers may arise from polyploid umbrella cells that have bypassed this senescent barrier. The editorial also discusses implications for cancer therapy. Many anticancer treatments induce senescence and polyploidization in tumor cells. Although this approach can initially suppress proliferation, some polyploid cancer cells may later adapt, reduce their ploidy, and resume division, contributing to relapse and treatment resistance. Understanding how polyploidy and senescence interact may therefore inform therapeutic strategies. Overall, the authors emphasize the need to study polyploidy and senescence together rather than in isolation. Integrating ploidy assessment into large-scale mapping efforts of senescent cells may improve insight into aging biology, tumor initiation, and resistance to therapy. DOI: https://doi.org/10.18632/aging.206355 Corresponding author: Iman M. Al-Naggar - alnaggar@uchc.edu Introduction video - https://www.youtube.com/watch?v=3Cl-JoV-j0o https://www.Aging-US.com​​ MEDIA@IMPACTJOURNALS.COM
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    4 Min.
  • How Aging Leads to Chronic Disease: A Two-Stage Model

    How Aging Leads to Chronic Disease: A Two-Stage Model
    Feb 17 2026
    Aging has long been explained in different ways. One traditional view is that it results from the gradual accumulation of molecular damage over time. Another perspective, based on evolutionary theory, suggests that natural selection strongly protects health during youth and reproductive years but becomes less effective later in life. As a result, biological effects that appear in older age may persist because they have little impact on reproduction. Over the past two decades, researchers have also explored the idea that biological programs beneficial early in life may continue operating later in ways that become harmful. Processes that once supported growth, repair, and reproduction may, with time, contribute to chronic disease. A recent review article, titled “Aging as a multifactorial disorder with two stages,” published in Aging-US by researchers at University College London and Queen Mary University of London, brings these different perspectives together into a unified model, to propose a broader explanation of how aging-related diseases develop. The review appears in a special issue honoring the late scientist Misha Blagosklonny, whose theoretical work on programmatic aging significantly influenced the field. Full blog - https://aging-us.org/2026/02/how-aging-leads-to-chronic-disease-a-two-stage-model/ Paper DOI - https://doi.org/10.18632/aging.206339 Corresponding author - David Gems - david.gems@ucl.ac.uk Abstract video - https://www.youtube.com/watch?v=d4TSI4Ot3yM Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206339 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, C. elegans, disease, hyperfunction, multifactorial model 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
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    7 Min.
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