Cellular senescence is a state of permanent cell cycle arrest triggered by stress, DNA damage, telomere shortening, or oncogenic signaling. Senescent cells remain metabolically active but exhibit altered gene expression and secrete pro-inflammatory factors known as the senescence-associated secretory phenotype (SASP). Accumulation of senescent cells contributes to tissue dysfunction, chronic inflammation, and age-related diseases. While senescence plays beneficial roles in development, wound healing, and tumor suppression, its persistence with age becomes detrimental. Targeting senescent cells through senolytic or senomorphic therapies is a promising strategy to improve healthspan and mitigate aging-related decline.
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Kenneth R Pelletier, University of California School of Medicine, United States
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Thomas J Webster, Brown University, United States
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