Mechanism

Cellular senescence

Cellular senescence is a state in which damaged cells permanently stop dividing but stay metabolically active, releasing inflammatory signals. Their build-up is a recognised hallmark of ageing.

Also known as: senescent cells, senescence, cellular senescence, SASP, senescence-associated secretory phenotype, zombie cells

What cellular senescence is

Cellular senescence is a stable form of cell-cycle arrest: a cell that has been stressed or damaged stops dividing for good, yet does not die. Instead it remains active and secretes a mix of inflammatory proteins known as the senescence-associated secretory phenotype (SASP).

Why it matters for longevity

A controlled amount of senescence is useful — it suppresses tumours and aids wound healing. But senescent cells accumulate with age, and their SASP fuels chronic low-grade inflammation (“inflammaging”) that damages neighbouring tissue. Senescent-cell burden is one of the hallmarks of aging and the direct target of senolytic drugs.

What the evidence shows

In animal models, clearing senescent cells or blocking specific SASP signals (for example interleukin-11) extends healthspan and, in some studies, lifespan. In humans the concept is well established biologically, but interventions that target senescence are still experimental.

Related ideas

Senescence connects to inflammation, the epigenetic clock (senescent cells show altered DNA methylation), and most directly to senolytic and senomorphic drug strategies.

Sources & references

  1. Widjaja AA, et al. Inhibition of IL-11 signalling extends mammalian healthspan and lifespan. Nature. 2024. doi:10.1038/s41586-024-07701-9
  2. López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. Hallmarks of aging: an expanding universe. Cell. 2023. doi:10.1016/j.cell.2022.11.001

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Educational information, not medical advice. Evidence ratings follow our methodology.