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One of my favorite new stories in the biology of aging is the body of work demonstrating an unexpected (to my mind, anyway) relationship between telomere length and various “organism-scale�? phenomena, e.g., psychological stress and cardiovascular disease (CVD). Two recent reviews extend the discussion. Kajstura et al. focus directly on cellular senescence, which can be induced both by telomeric shortening and genotoxic damage, in cardiac progenitor cells. Does senescence play a role in cardiovascular aging and the age-related onset of CVD?
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