Abstract
Physical exercise, a potent functional intervention in protecting against cardiovascular diseases, is a hot topic in recent years. Exercise has been shown to reduce cardiac risk factors, protect against myocardial damage, and increase cardiac function. This improves quality of life and decreases mortality and morbidity in a variety of cardiovascular diseases, including myocardial infarction, cardiac ischemia/reperfusion injury, diabetic cardiomyopathy, cardiac aging, and pulmonary hypertension. The cellular adaptation to exercise can be associated with both endogenous and exogenous factors: (1) exercise induces cardiac growth via hypertrophy and renewal of cardiomyocytes, and (2) exercise induces endothelial progenitor cells to proliferate, migrate and differentiate into mature endothelial cells, giving rise to endothelial regeneration and angiogenesis. The cellular adaptations associated with exercise are due to the activation of several signaling pathways, in particular, the growth factor neuregulin1 (NRG1)-ErbB4-C/EBPβ and insulin-like growth factor (IGF)-1-PI3k-Akt signaling pathways. Of interest, microRNAs (miRNAs, miRs) such as miR-222 also play a major role in the beneficial effects of exercise. Thus, exploring the mechanisms mediating exercise-induced benefits will be instrumental for devising new effective therapies against cardiovascular diseases.
Highlights
Cardiovascular disease (CVD) is the leading cause of death worldwide and exerts a considerable emotional and economic burden [1, 2]
We summarize the protective effects of exercise against cardiac injury and address the underlying cellular and molecular mechanisms
We provide an overview of both exercise-induced cardiac hypertrophy and renewal, and exercise-induced mobilization of Endothelial progenitor cells (EPCs) to proliferate, migrate and differentiate into mature endothelial cells capable of regeneration and angiogenesis as primary contributors
Summary
Cardiovascular disease (CVD) is the leading cause of death worldwide and exerts a considerable emotional and economic burden [1, 2]. Exercise has been reported to effectively reduce cardiovascular morbidity and mortality [4]. A study showed that compared to no physical exercise at all, any level of leisure-time physical exercise is associated with decreased rate of sudden death [5]. Those who do less exercise than recommended in the “2008 physical activity guidelines for Americans” still have a 20% lower rate of sudden death. It appears evident that exercise may confer a cardioprotective phenotype, the strength of the effects and the underlying mechanisms remain elusive
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