A cell becomes senescent when it detects damage it cannot repair: telomeres that are too short, DNA lesions, intense oxidative stress or oncogene activation. Stopping is a defence against cancer, because it prevents a damaged cell from continuing to multiply.
The problem is what it does afterwards. Senescent cells secrete a mix of cytokines, enzymes and growth factors called the SASP (senescence-associated secretory phenotype), which sustains low-grade inflammation and can push neighbouring cells into the same state. With age they build up in many tissues.
That is why senescence is a central topic in ageing research, with lines of work that aim to remove these cells (“senolytic” drugs) or modulate their secretions. Telomere shortening is one of its best-studied causes.
Many compounds associated with “longevity” are studied for their relationship with senescence or telomeres. It is an active field, but much of the evidence is still preclinical.
Related terms
Related catalogue compounds
Definition for educational and scientific purposes. It is not medical advice or a recommendation for use. NeoPeptidos products are sold labelled for research use only (RUO).