Length-independent telomere damage drives cardiomyocyte senescence

Ageing is the biggest risk factor to cardiovascular health and is associated with increased incidence of cardiovascular disease. Cellular senescence, a process driven in part by telomere shortening has been implicated in age-related cardiac dysfunction. However, the role of cellular senescence and its underlying mechanisms in slowly dividing/post-mitotic cardiomyocytes is not understood. Overall design: We quantify transcription via high throughput RNA sequencing in young (3 months) and old (20 months) mouse cardiomyocytes.