Effect of exercise-induced irisin on myocardial fibrosis / 中国组织工程研究

ABSTRACT

BACKGROUND: Myocardial fibrosis is an important topic in modern medical research, and its development is closely related to common heart diseases such as arrhythmia and chronic heart failure. Exercise intervention can significantly improve myocardial fibrosis, but there is no systematic and comprehensive understanding of the mechanism by which exercise improves myocardial fibrosis as well as the effects of different types of exercises on myocardial fibrosis. To date, it is still unclear about how exercise triggers the production of irisin against myocardial fibrosis. OBJECTIVE: To comprehensively review the exercise-induced production of irisin and its effect on myocardial fibrosis, and reveal its myocardial protection, so as to improve heart function and provide fundamental basis for preventing against common heart diseases, such as arrhythmia and chronic heart failure. METHODS: A search of ELSEVIER, Web of Science, CNKI, WanFanga, VIP and Taiwan Academic Literature Database was performed for articles regarding exercise, irisin, and myocardial fibrosis. The deadline for publication was August 2019. According to the inclusion and exclusion criteria, 58 articles were eligible for review. RESULTS AND CONCLUSION: Long-term and single exercise in human experiments has been shown to improve muscular and circulatory irisin levels, which has been better verified in animal experiments. A few experimental results indicate that long-term exercise has no significant effect on blood irisin levels, which may be due to different research subjects, exercise methods, exercise intensity, and exercise frequency. However, the specific mechanism is still unclear. Exercise can improve myocardial fibrosis by acting on myocardial mitochondrial stabilization, energy metabolism, oxidative stress and inflammatory response. The occurrence of myocardial fibrosis results from the regulation of neuroendocrine and oxidative stress and inflammatory responses. Irisin can influence the processes of oxidative stress and inflammation related to the mechanism of myocardial fibrosis, by inhibiting ROS/p38MAPK/NF-κB signaling pathway, endogenous reactive oxygen species and ROS-NLRP3 inflammation signaling pathway, and regulating the expression of uncoupling protein 2 and mitochondrial homeostasis. Therefore, exercise may improve myocardial fibrosis by upregulating the expression of irisin, thus providing myocardial protection.