Aerobic Exercise Attenuates Pressure Overload–Induced Myocardial Remodeling and Myocardial Inflammation via Upregulating miR-574-3p in Mice

作者：Qiaoying Chen, Yi-Na Jiang, Xuan Guan, Fangfang Ren, Shujie Wu, Maoping Chu, Lianpin Wu, Teng-Fang Lai, Lei Li · 发表于：Circulation Heart Failure · 年份：2024 · DOI：10.1161/circheartfailure.123.010569 · 被引用次数：21 · 研究领域：Cardiac Fibrosis and Remodeling、Cardiovascular Function and Risk Factors、MicroRNA in disease regulation

BACKGROUND: Exercise training can promote cardiac rehabilitation, thereby reducing cardiovascular disease mortality and hospitalization rates. MicroRNAs (miRs) are closely related to heart disease, among which miR-574-3p plays an important role in myocardial remodeling, but its role in exercise-mediated cardioprotection is still unclear. METHODS: A mouse myocardial hypertrophy model was established by transverse aortic coarctation, and a 4-week swimming exercise training was performed 1 week after the operation. After swimming training, echocardiography was used to evaluate cardiac function in mice, and histopathologic staining was used to detect cardiac hypertrophy, myocardial fibrosis, and cardiac inflammation. Quantitative real-time polymerase chain reaction was used to detect the expression levels of miR-574-3p and cardiac hypertrophy markers. Western blotting detected the IL-6 (interleukin-6)/JAK/STAT inflammatory signaling pathway. RESULTS: Echocardiography and histochemical staining found that aerobic exercise significantly improved pressure overload-induced myocardial hypertrophy (n=6), myocardial interstitial fibrosis (n=6), and cardiac inflammation (n=6). Quantitative real-time polymerase chain reaction detection showed that aerobic exercise upregulated the expression level of miR-574-3p (n=6). After specific knockdown of miR-574-3p in mouse hearts with adeno-associated virus 9 using cardiac troponin T promoter, we found that the protective effect of exercise traini...