So it turns out that replicative senescence, the process by which short telomeres arrest division, activates autophagy as a mechanism to prevent uncontrolled replicaton and chromosome damage (leading to cancer), whereas DNA damage away from the telomere activates apoptosis (if not repaired).
https://www.scienced...90123131706.htm
https://www.nature.c...1586-019-0885-0
(Abstract only)