•My
current view is that telomere lengths
are downstream consequences of
other cell state factors. Telomeres
generally shorten with cell reproduction
but can also lengthen depending on complex feedback loops. Cell
senescence can lead to short telomeres which can contribute to, apoptosis, or malignant transformation. Cell senescence is largely driven by other factors than telomere lengths.
•Three years
ago, I subscribed to the notion that extending telomere lengths could be a iife-extending intervention, but no longer do.
•Because rats and mice have long telomeres throughout
life, telomere shortening
by itself does not fully explain mammalian aging.