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Cellular senescence, a process driven in part by telomere shortening, has been implicated in age\u2010related tissue dysfunction. Here, we address the question of how senescence is induced in rarely dividing\/post\u2010mitotic cardiomyocytes and investigate whether clearance of senescent cells attenuates age\u2010related cardiac dysfunction. During ageing, human and murine cardiomyocytes acquire a senescent\u2010like phenotype characterised by persistent DNA damage at telomere regions that can be driven by mitochondrial dysfunction and crucially can occur independently of cell division and telomere length. Length\u2010independent telomere damage in cardiomyocytes activates the classical senescence\u2010inducing\u00a0pathways, p21\n                    <jats:sup>CIP<\/jats:sup>\n                    and p16\n                    <jats:sup>INK4a<\/jats:sup>\n                    , and results in a non\u2010canonical\u00a0senescence\u2010associated secretory phenotype, which is pro\u2010fibrotic and pro\u2010hypertrophic. Pharmacological or genetic clearance of senescent cells in mice alleviates detrimental features of cardiac ageing, including myocardial hypertrophy and fibrosis. Our data describe a mechanism by which senescence can occur and contribute to age\u2010related myocardial dysfunction and in the wider setting to ageing in post\u2010mitotic tissues.\n                  <\/jats:p>","DOI":"10.15252\/embj.2018100492","type":"journal-article","created":{"date-parts":[[2019,2,8]],"date-time":"2019-02-08T15:53:40Z","timestamp":1549641220000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":509,"title":["Length\u2010independent telomere damage drives post\u2010mitotic cardiomyocyte 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