Stress-induced senescence is triggered by cellular stressors independent of cell division, including oxidative stress, DNA damage, radiation, oncogene activation, and mitochondrial dysfunction. Unlike replicative senescence, this form can occur rapidly in both dividing and non-dividing cells. Stress-induced senescence acts as a protective response to prevent damaged cells from proliferating, thereby reducing cancer risk. However, persistent stress-induced senescence contributes to tissue dysfunction and chronic inflammation during aging. These senescent cells often display a strong SASP, amplifying inflammatory signaling and promoting aging in surrounding tissues. Stress-induced senescence links environmental exposures, metabolic imbalance, and lifestyle factors directly to biological aging, making it a key focus in preventive aging research.
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