Telomere attrition is not a replicative limit—it's a DNA damage signal that triggers senescence prematurely

We think cells stop dividing because telomeres get too short. But cells can divide thousands more times before telomeres truly run out.

The actual trigger: when telomeres become critically short, they're recognized as DNA damage. p53 activates, cell cycle arrests.

It's not that the cell ran out of telomere. It's that the cell decided the telomere was damaged and initiated senescence as a safety response.