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In most somatic mammalian cell types extensive replication and various types of cellular insults induce a permanent form of growth arrest called senescence. Senescence has been comprehensively characterised in cell culture, but its occurrence in vivo has only recently started to become appreciated. In this mini-review, we examine the evidence for the occurrence of senescence in vivo, with particular emphasis on the cardiovascular system. We also describe the senescent phenotype and discuss its pathophysiological implications. We examine findings in animal models of ageing and human genetic disorders that argue for and against a role of senescence in age-related pathologies in general and vascular disease in particular.