That’s a really good question and one I tried to answer in my 2013 paper (I don’t publish much). My conclusion based on the work of Lapasset is that if you rejuvenate a cell – using transcription factors to change them (some) to induced pleuripotent cells- not only does their mitochondrial functioning return to normal and they stop producing ROS but their telomeres grow long again (and experiments have shown that the procedures didn’t select for long telomered cells to be induced to pleuripotence. My conclusion is that there’s no mechanism preventing telomerase from lengthening telomeres – other than the body signals not to do so. None of this damage is other than purposeful. My solution is to convince the body that’s its young again, and it will act accordingly (to oversimplify a bit). That shortening telomeres cause many age-related conditions I have no doubt – but I think it’s long known that the strict “end-replication problem’ to explain replicative
senescence as envisioned by Olivnikov, where each cell division shortens the telomeres isn’t the truth – or at least it isn’t the way it has to be.