Abstract
Introduction: Telomere shortening is associated with acceleration of ageing, chronic disease, and mortality in humans. Mutations that predispose to a failure to maintain telomere length induce a premature decline in organ homeostasis and a shortened lifespan in human and mice. Upon reaching a critically short length, dysfunctional telomeres activate the ATM/p53 DNA damage pathway and its downstream target p21, which induces a permanent G1 cell cycle arrest in primary human cells known as senescence.
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