Cellular senescence

What it is

When a cell sustains damage it cannot repair, one option is permanent arrest. It stops dividing but does not die, resists apoptosis, enlarges, and changes what it secretes. That is senescence, and it is protective in the short term because it prevents damaged cells from replicating.

The problem is the secretion. Senescent cells release a mix of inflammatory cytokines, growth factors and proteases known as the senescence-associated secretory phenotype, which pushes neighboring cells toward dysfunction and senescence in turn.

Why it matters with age

Senescent cells accumulate in aged tissue, partly because immune clearance becomes less efficient. Transplanting a relatively small number of senescent cells into young mice is enough to cause physical dysfunction, which is unusually direct evidence of causation.

This is one of the more mechanistically satisfying links between molecular damage and the chronic low grade inflammation that tracks aging in people.

How it is detected

There is no single marker. Identification relies on a combination: loss of proliferation, raised p16 and p21, senescence-associated beta-galactosidase activity, and the secretory profile. Guidance from the field explicitly warns against relying on any one of these.

There is no validated blood test that tells an individual their senescent cell burden. No consumer test has been validated for that purpose.

References

1. Gorgoulis V, et al. Cellular senescence: defining a path forward. Cell. 2019.
2. Xu M, et al. Senolytics improve physical function and increase lifespan in old age. Nat Med. 2018.
3. Campisi J. Aging, cellular senescence, and cancer. Annu Rev Physiol. 2013.