Abstract
Aging is a prominent risk factor for cardiovascular diseases, which is the leading cause of death around the world. Recently, cellular senescence has received potential attention as a promising target in preventing cardiovascular diseases, including acute myocardial infarction, atherosclerosis, cardiac aging, pressure overload-induced hypertrophy, heart regeneration, hypertension, and abdominal aortic aneurysm. Here, we discuss the mechanisms underlying cellular senescence and describe the involvement of senescent cardiovascular cells (including cardiomyocytes, endothelial cells, vascular smooth muscle cells, fibroblasts/myofibroblasts and T cells) in age-related cardiovascular diseases. Then, we highlight the targets (SIRT1 and mTOR) that regulating cellular senescence in cardiovascular disorders. Furthermore, we review the evidence that senescent cells can exert both beneficial and detrimental implications in cardiovascular diseases on a context-dependent manner. Finally, we summarize the emerging pro-senescent or anti-senescent interventions and discuss their therapeutic potential in preventing cardiovascular diseases.
Highlights
Aging is a determinant risk factor for cardiovascular diseases, which is the leading cause of death around the world
In contrast to replicative senescence, stress-induced premature senescence (SIPS) is another type of cellular senescence that can be triggered by various external stimuli independent of telomere length, including persistent DNA damage, telomere dysfunction, mitochondrial dysfunction and oxidative stress
Substantial experimental evidence suggests that activation of DNA-damage response (DDR) with DNA double strand breaks (DSBs) is a major determinant for age-associated pathophysiological changes and all stressors that result in persistent DNA damage can induce a senescent phenotype [21]
Summary
Aging is a determinant risk factor for cardiovascular diseases, which is the leading cause of death around the world. The complex interactions between cardiovascular aging processes and various risk factors (e.g., hypertension, myocardial infarction, atherosclerosis and fibrosis) inevitably contribute to the development of heart failure. The telomere length-independent senescence was observed in many aged or damaged tissues. Such stress-induced premature senescence (SIPS) can be triggered by distinctive stressful stimuli, including persistent DNA damage, oncogene activation, oxidative stress and mitochondrial dysfunction in cardiovascular system [7,8]. Cellular senescence in cardiovascular diseases arrest, the senescent cells are differed from other nondividing cells (such as quiescent cells) with specific morphological and functional features. We first discuss the mechanisms and the features underlying cellular senescence. We focus on the emerging pro-senescent and antisenescent therapies and discuss their therapeutic potential for cardiovascular diseases
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