Senescence

Cellular senescence is a state of stable, irreversible cell cycle arrest in which cells remain metabolically active but permanently cease dividing. Senescence can be triggered by telomere shortening, DNA damage, oncogene activation, oxidative stress, or mitochondrial dysfunction. While senescence initially serves protective functions by preventing damaged cells from proliferating, the accumulation of senescent cells with age becomes pathological. Senescent cells secrete a complex mixture of pro-inflammatory cytokines, chemokines, and proteases known as the senescence-associated secretory phenotype (SASP), which drives chronic inflammation and tissue dysfunction. NAD+ decline promotes senescence by impairing sirtuin-mediated stress responses and DNA repair, while NAD+ supplementation research aims to delay senescence onset by maintaining cellular repair capacity.