Cellular senescence is a permanent cell-cycle arrest triggered by DNA damage, oncogene activation, oxidative stress, or telomere shortening. Senescent cells stop dividing but resist apoptosis.
Mechanism — Senescent cells secrete a pro-inflammatory mix called the SASP (senescence-associated secretory phenotype) — cytokines, chemokines, MMPs. Drives local and systemic inflammation, impairs nearby tissue function, and recruits immune cells.
Use case — Promote senolysis (senescent cell clearance) via exercise, fasting, and emerging compounds (fisetin, dasatinib + quercetin combo, FOXO4-DRI). Adequate sleep and reduced chronic stress lower senescent burden.
Caveats — Some senescence is protective — total elimination isn't the goal. Targeted, periodic clearance of harmful senescent cells is the emerging strategy. Don't take aggressive senolytic protocols without medical oversight.