Senescent cells stop dividing but don't die — instead they secrete a senescence-associated secretory phenotype (SASP) of inflammatory signals that can push nearby healthy cells toward senescence too.
senescence triggered when damage > threshold
SASP spread ~ senescentCount * secretionRate
- Tissue cells — the resident cell population in the modeled tissue patch.
- Damage-prone sites — locations where DNA damage or telomere shortening accumulates fastest (e.g. high-turnover epithelium).
- Damage accumulation rate — how quickly cellular stress (oxidative damage, replication stress) pushes cells toward the senescence switch.
- Senolytic clearance — rate at which senescent cells are cleared, either by immune surveillance or senolytic drugs (dasatinib+quercetin).
Senolytic drugs that selectively kill senescent cells have extended healthspan in mouse models by removing the chronic SASP-driven inflammation that senescent cells spread to otherwise healthy neighboring tissue.