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Wounds may trigger 'aged' cells within hours, reshaping how senescence starts

Wounds may trigger 'aged' cells within hours, reshaping how senescence starts
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Wounds may trigger 'aged' cells within hours, reshaping how senescence starts Sadie Harley Scientific Editor Robert Egan Associate Editor What if a process we associate with aging actually helps the body heal? A study led by Mikolaj Ogrodnik, LBI Trauma, published in Nature Cell Biology, shows that cells enter a state of senescence within minutes to hours after an injury—and that this rapid response not only plays a key role in wound healing, but also changes the paradigm of how slowly...

Wounds may trigger 'aged' cells within hours, reshaping how senescence starts Sadie Harley Scientific Editor Robert Egan Associate Editor What if a process we associate with aging actually helps the body heal? A study led by Mikolaj Ogrodnik, LBI Trauma, published in Nature Cell Biology, shows that cells enter a state of senescence within minutes to hours after an injury—and that this rapid response not only plays a key role in wound healing, but also changes the paradigm of how slowly senescence was expected to arise. Cellular senescence is commonly linked to aging and chronic disease, and it has long been thought that cells need days to weeks to become senescent. However, this new publication challenges that notion. The research team demonstrates that, following skin injury, senescence can be dramatically accelerated and emerge within just a few hours. How cells switch to senescence fast Strikingly, this rapid response occurs independently of gene transcription. Instead of activating new genes, cells rely on pre-existing messenger RNA to quickly produce the protein p21, which then triggers senescence. In other words, one could say that our skin is ready for a potential injury by having stored molecules for rapid senescence induction—molecules which are not used unless wounding occurs. Early senescence shapes wound healing These rapidly emerging senescent cells are by no means passive. They release signaling molecules, guide the migration of cells to close the wound, and actively coordinate the early phases of wound healing. If this early senescence response is disrupted, healing slows down. In contrast, senescence at later stages has no beneficial effects anymore, which points to a narrow time window in which these cells are particularly important, as they are also effectively eliminated after healing is completed by the skin's natural behavior, one of which is shedding of cells with epithelium. "Since chronically persistent senescent cells are associated with many age-related diseases, their elimination after having been useful seems important to maintain health in tissues over the aging process," points out Mikolaj Ogrodnik. Global collaboration and future directions The study is the result of an international research collaboration between LBI Trauma, the Research Center in Cooperation with AUVA, and more than 10 partnering institutions, including the Mayo Clinic (U.S.), BOKU University, the Medical University of Vienna, Université Côte d'Azur (France), InLife—Polish Academy of Sciences, and the Chinese Academy of Sciences. Together, the results generated by these collaborating institutions challenge, but also advance our current understanding of senescence. Rather than being solely a hallmark of aging, senescence appears here as a fast and tightly regulated response to tissue damage. In the long term, these findings could help to improve healing processes by harnessing the very early cellular mechanisms the body naturally deploys after injury and better understand the state of cellular senescence in conditions such as diseases and aging. Publication details Karla Valdivieso et al, Transcription-independent induction of rapid-onset senescence is integral to healing, Nature Cell Biology (2026). DOI: 10.1038/s41556-026-01948-2 Journal information: Nature Cell Biology Provided by Ludwig Boltzmann Institute for Traumatology
Sadie Harley Scientific (ORG) Robert Egan (PERSON) Mikolaj Ogrodnik (PERSON) LBI (PERSON) Nature Cell Biology (ORG) the Research Center in Cooperation (ORG) AUVA (ORG) the Mayo Clinic (ORG) U.S. (LOCATION) BOKU University (ORG) the Medical University of Vienna (ORG) Université Côte d'Azur (ORG) France (LOCATION) Polish Academy of Sciences (ORG) the Chinese Academy of Sciences (ORG)
Originally published by Phys.org Read original →