Moderate exercise is an effective and economic way to prevent and treat cardiovascular diseases. Unlike pathological cardiac growth, exercise-induced cardiac growth, excluding extreme strenuous exercise, does not cause cardiac cell death, fibrosis, and cardiac dysfunction. The balanced cardiomyogenesis (cardiomyocyte hypertrophy and hyperplasia) and neo-angiogenesis are essential determinants for exercise-induced cardiac growth. In particular, exercise leads to physiological cardiac growth through regulating the IGF-1-PI3K-Akt, nitric oxide (NO), C/EBPβ, and PGC-1α signaling pathways, which might be novel therapeutic targets for cardiac diseases. The formation of new cardiomyocytes in response to exercise suggests that exercise might be a useful tool to enhance cardiac regenerative capacity. Exercise also exerts its protective effects against cardiac aging and cardiac metabolic derangement. Moreover, growing evidence reveals the regulation of cardiac and circulating microRNAs in response to exercise. A better understanding of the mechanisms underlying exercise-induced cardioprotection will lead to the development of innovative pharmacotherapies for cardiac diseases.
Keywords: Exercise, cardiac growth, regeneration, aging, metabolism, microRNA.
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