Cellular senescence

Assembled from 17 blocks · 2 evidence · 12 related

1. Story
2. A stable arrest of cell division in which the cell remains metabolically active and secretes a characteristic mixture of inflammatory cytokines, proteases and growth factors known as the senescence-associated secretory phenotype. It is not simply cell death or exhaustion: it is a programme, triggered by telomere attrition, DNA damage, oncogene activation or other stress, and it is protective in the short term — it is one of the body's principal anti-cancer mechanisms and a component of wound healing. Its origins lie in Leonard Hayflick and Paul Moorhead's 1961 demonstration that normal human diploid fibroblasts divide only a limited number of times in culture, which refuted the then-prevailing belief that cells were intrinsically immortal. Senescent cells accumulate with age; in mice, genetically clearing them delays several age-related pathologies. Whether their accumulation is a cause of human ageing, a consequence of it, or both, is not settled, and no assay reliably counts senescent cells in a living human being.
3. Knowledge
4. Cellular senescence
5. The hallmarks of ageing
6. Connections
7. The hallmarks of ageing
8. Senolytics
9. Human diploid cells are shown to have a finite replicative capacity
10. The hallmarks of ageing are formalised
11. The first senolytic drugs are identified
12. Cellular senescence
13. Model organism lifespan research
14. The hallmarks of ageing are formalised
15. Evidence
16. Supports the finite replicative capacity of normal human diploid fibroblasts and the refutation of indefinite culture. V55 verification basis: not retrieved in this session.
17. Supports the hallmark framework, its three inclusion criteria and the expansion from nine to twelve hallmarks. V55 verification basis: neither paper was retrieved; the enumerated hallmark list must be checked against the originals.