par Shakeri, Hadis 
;Lemmens, Katrien;Gevaert, Andreas B;De Meyer, Guido R Y;Segers, Vincent F M
Référence American journal of physiology. Heart and circulatory physiology, 315, 3, page (H448-H462)
Publication Publié, 2018-12-01
;Lemmens, Katrien;Gevaert, Andreas B;De Meyer, Guido R Y;Segers, Vincent F MRéférence American journal of physiology. Heart and circulatory physiology, 315, 3, page (H448-H462)
Publication Publié, 2018-12-01
Article révisé par les pairs
| Résumé : | Aging is a powerful independent risk factor for cardiovascular diseases such as atherosclerosis and heart failure. Concomitant diabetes mellitus strongly reinforces this effect of aging on cardiovascular disease. Cellular senescence is a fundamental mechanism of aging and appears to play a crucial role in the onset and prognosis of cardiovascular disease in the context of both aging and diabetes. Senescent cells are in a state of cell cycle arrest but remain metabolically active by secreting inflammatory factors. This senescence-associated secretory phenotype is a trigger of chronic inflammation, oxidative stress, and decreased nitric oxide bioavailability. A complex interplay between these three mechanisms results in age- and diabetes-associated cardiovascular damage. In this review, we summarize current knowledge on cellular senescence and its secretory phenotype, which might be the missing link between aging and diabetes contributing to cardiovascular disease. |
