Abstract
Loss of cardiomyocytes is a vital manifestation and predisposing factor of many cardiovascular diseases and will eventually lead to heart failure (HF). On the other hand, adult mammalian cardiomyocytes have a very limited regenerative capacity and cannot achieve self-repair of the myocardium after injury. Therefore, it is necessary to promote regeneration and repair of the myocardium through effective intervention means. Exercise plays an important role in the prevention and rehabilitation of cardiovascular diseases. Exercise can improve ischemia-reperfusion injury, reduce the size of the infarcted area, and improve the quality of life of patients. In addition, exercise has also been shown to be able to elevate the proliferative potential of adult cardiomyocytes and promote myocardial regeneration. Studies have shown that newly formed cardiomyocytes in adult mammalian hearts are mainly derived from pre-existing cardiomyocytes. By regulating various cytokines, transcription factors, and microRNAs (miRNAs), exercise can promote the dedifferentiation and proliferation of pre-existing cardiomyocytes to form new cardiomyocytes. Therefore, this paper focuses on the recent research progress of exercise-induced adult cardiomyocyte proliferation and explores its potential molecular mechanism.
Highlights
Heart failure (HF) is an advanced stage of various cardiac diseases, placing a heavy burden on the human social health care system (Ziaeian and Fonarow, 2016)
We focus on the recent findings and possible mechanisms of exercise-promoted cardiomyocyte proliferation in order to provide a reference for further research and clinical application
Studies have found that resistance exercise after myocardial infarction in rats can significantly up-regulate the protein expression of FSTL1 and its receptor DIP2A, effectively activate the PI3K/Akt pathway and significantly increase the protein expression of CyclinD1 and CDK4 (Tian et al, 2018); At the same time, resistance exercise after infarction increased the number of cardiomyocyte with proliferative activity, significantly increased the percentage of cardiomyocyte proliferation, and significantly improved cardiac function (Tian et al, 2018); the above evidence suggests that resistance exercise may play
Summary
Heart failure (HF) is an advanced stage of various cardiac diseases, placing a heavy burden on the human social health care system (Ziaeian and Fonarow, 2016). Among them, using a variety of stem and progenitor cells to induce differentiation into cardiomyocytes has been considered a possible mechanism for cardiac repair after myocardial injury (Williams et al, 2013; Zhang et al, 2015). This stem cell therapy has been gradually applied in clinical practice (Cahill et al, 2017; Sheng et al, 2019), there is still some controversy about its efficacy (Gyöngyösi et al, 2015). We focus on the recent findings and possible mechanisms of exercise-promoted cardiomyocyte proliferation in order to provide a reference for further research and clinical application
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