Abstract
Exercise training has been reported to ameliorate heart dysfunction in both humans and animals after myocardial infarction (MI). Exercise-induced cardioprotective factors have been implicated in mediating cardiac repair under pathological conditions. These protective factors secreted by or enriched in the heart could exert cardioprotective functions in an autocrine or paracrine manner. Extracellular vesicles, especially exosomes, contain key molecules and play an essential role in cell-to-cell communication via delivery of various factors, which may be a novel target to study the mechanism of exercise-induced benefits, besides traditional signaling pathways. This review is designed to demonstrate the function and underlying protective mechanism of exercise-induced cardioprotective factors in MI, with an aim to offer more potential therapeutic targets for MI.
Highlights
Myocardial infarction (MI) is a serious result of cardiovascular disease and the leading cause of mortality and morbidity (Andersson et al, 2018)
This review summarizes the protective role and underlying mechanism of cardiac-derived protective factors that can be induced by exercise in myocardial infarction (MI), with an aim to demonstrate their potential as therapeutic targets (Figure 1)
Shen et al (2019) showed that FSTL1 expression declined dramatically in hypoxia-induced mesenchymal stem cells (MSCs), while overexpression of FSTL1 significantly prolonged MSC retention after implantation in the ischemic myocardium, thereby preserving heart function after MI by limiting scar formation, reducing inflammatory response, and enhancing neovascularization. These findings suggest that FSTL1 might serve as a key therapeutic target for MI
Summary
Myocardial infarction (MI) is a serious result of cardiovascular disease and the leading cause of mortality and morbidity (Andersson et al, 2018). Shen et al (2019) showed that FSTL1 expression declined dramatically in hypoxia-induced mesenchymal stem cells (MSCs), while overexpression of FSTL1 significantly prolonged MSC retention after implantation in the ischemic myocardium, thereby preserving heart function after MI by limiting scar formation, reducing inflammatory response, and enhancing neovascularization. These findings suggest that FSTL1 might serve as a key therapeutic target for MI. Liao et al (2019) reported that treatment with irisin for 2 weeks significantly reduced infarct size and fibrosis in MI mice, significantly increased angiogenesis in the ischemic area, and decreased cardiomyocyte apoptosis via activating the ERK signaling pathway. It has been shown that injection of MI mice with recombinant interleukin (IL)-22 in the 1st week after acute MI effectively prevents left ventricular
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