Cellular senescence
Damaged cells stop dividing but remain active, secreting factors that harm surrounding tissue.
Senescent cells accumulate via telomere attrition, DNA damage, and oncogenic stress. The senescence-associated secretory phenotype (IL-6, IL-8, MMPs) drives paracrine dysfunction, inflammaging, and stem-cell niche disruption.
How to minimize cellular senescence
- Primary prevention: reduce DNA-damage and chronic inflammation sources that increase senescent cell burden early.
- Senolytics (dasatinib + quercetin, fisetin) clear senescent cells in pilot human studies—long-term safety and efficacy for healthy aging unproven.
- Senomorphics (rapamycin, JAK inhibitors) suppress SASP without ablation—still investigational.
- Exercise may lower senescent cell markers in adipose and muscle in rodent and some human biopsy data.