I’m not sure of what your answer is I think that everything you say about telomeres can be said about DNA damage – example
DNA damage leads to loss of stem cells and the renewal of tissue that they offer.
DNA damages lead to senescent cells which increase inflammation in the body by emitting inflammatory cytokines.
DNA damages lead to chromosome instability, double stranded breaks that can lead to cancer.
DNA damage in hematopoietic stem cells reduces production of new white blood cells, contributing both to cancer and to vulnerability to infectious disease
So is DNA damage a cause or a result of aging? To my mind it’s the proximate cause of aging – but not the effective cause – that ‘supreme’ cause results from turning down DNA repair later in life. When you say, ” removing cells with short telomeres increases mouse life span substantially.” what are you referring to? In any case, since critical length telomeres induce the DNA damage response (DDR), even in distally located cells of different organs, removing cells with DNA damage (the sort that would stimulate the DDR) should also increase lifespan. So yes, there’s no doubt that telomere shortening leads to aging – but the question is why the telomere shortening? It’s been ‘traditional’ to accept that the end replication problem is the reason, but we know that the cell can alter the length of its telomeres; the cell could if it ‘wanted to’ regrow its telomeres (as mice cells regularly do) – but it doesn’t.