Myocardial aging involves cellular senescence, mitochondrial dysfunction, and extracellular matrix remodeling, which contribute to age-related cardiac diseases and potential therapeutic targets.
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Population aging is becoming an increasingly large-scale and significant global challenge. Aging is accompanied by a growing prevalence of a constellation of cardiovascular diseases, among which coronary heart disease, atrial fibrillation, and ventricular tachyarrhythmias hold leading positions. Myocardial aging is associated with a number of diverse mechanisms, including the accumulation of senescent cells and remodeling of the extracellular matrix at the tissue level, as well as mitochondrial dysfunction, impaired autophagy, oxidative stress, and DNA damage at the cellular level. This review provides a comprehensive analysis of the cellular and molecular mechanisms underlying the aging of the myocardium and the cardiovascular system as a whole. A special focus is on the processes of cellular senescence, the formation of the senescence-associated secretory phenotype (SASP), structural and functional alterations in cardiovascular system cells that precede the development of age-related cardiac diseases, as well as promising methods of overcoming aging.
Filatova et al. (Sun,) reported a other. Myocardial aging involves cellular senescence, mitochondrial dysfunction, and extracellular matrix remodeling, which contribute to age-related cardiac diseases and potential therapeutic targets.