Définition
Cellular senescence is a state of permanent cell cycle arrest in which a cell can no longer divide but remains metabolically active. Senescent cells accumulate with age and secrete inflammatory molecules (the SASP) that drive tissue dysfunction, chronic inflammation, and accelerated biological aging.
Cellular senescence was first described by Leonard Hayflick in 1961, who observed that normal human cells divide a finite number of times (the Hayflick limit) before entering permanent growth arrest. This is now understood to be driven primarily by telomere shortening — when telomeres reach critical length, they trigger a DNA damage response that arrests the cell cycle.
Senescence can also be triggered by other stressors: oncogenic mutations (as a tumor-suppressive mechanism), oxidative stress, radiation, and accumulated DNA damage. In this context, senescence is initially protective — preventing damaged cells from proliferating uncontrollably.
The problem is the accumulation of senescent cells in aging tissues. Senescent cells are not simply inactive — they secrete a complex mixture of cytokines, chemokines, and proteases called the senescence-associated secretory phenotype (SASP). The SASP drives chronic inflammation, degrades the extracellular matrix, impairs neighboring cell function, and can induce senescence in nearby healthy cells (bystander senescence). This positions senescent cell accumulation as a key driver of inflammaging and tissue aging.
Natural compounds with research interest for reducing senescent cell burden include fisetin (a flavonoid concentrated in strawberries), quercetin (found in onions, capers, and apples), and piperlongumine. The field is moving rapidly; human evidence remains preliminary but mechanistically compelling.
Termes associés
Ava Longevity · Built on the Ava Method · MMXXV