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Postinfarction exercise training alleviates cardiac dysfunction and adverse remodeling via mitochondrial biogenesis and SIRT1/PGC‐1α/PI3K/Akt signaling
Author(s) -
Jia Dandan,
Hou Lu,
Lv Yongzhi,
Xi Lei,
Tian Zhenjun
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28939
Subject(s) - mitochondrial biogenesis , cardioprotection , medicine , endurance training , cardiology , protein kinase b , oxidative stress , cardiac function curve , myocardial infarction , endocrinology , ventricular remodeling , mitochondrion , cardiac fibrosis , fibrosis , signal transduction , biology , heart failure , microbiology and biotechnology
Exercise training mitigates cardiac pathological remodeling and dysfunction caused by myocardial infarction (MI), but its underlying cellular and molecular mechanisms remain elusive. Our present study in an in vivo rat model of MI determined the impact of post‐MI exercise training on myocardial fibrosis, mitochondrial biogenesis, antioxidant capacity, and ventricular function. Adult male rats were randomized into: (a) Sedentary control group; (b) 4‐week treadmill exercise training group; (c) Sham surgery group; (d) MI group with permanent ligation of left anterior descending coronary artery and kept sedentary during post‐MI period; and (e) post‐MI 4‐week exercise training group. Results indicated that exercise training significantly improved post‐MI left ventricular function and reduced markers of cardiac fibrosis. Exercise training also significantly attenuated MI‐induced mitochondrial damage and oxidative stress, which were associated with enhanced antioxidant enzyme expression and/or activity and total antioxidant capacity in the heart. Interestingly, the adaptive activation of the SIRT1/PGC‐1α/PI3K/Akt signaling following MI was further enhanced by post‐MI exercise training, which is likely responsible for exercise‐induced cardioprotection and mitochondrial biogenesis. In conclusion, this study has provided novel evidence on the activation of SIRT1/PGC‐1α/PI3K/Akt pathway, which may mediate exercise‐induced cardioprotection through reduction of cardiac fibrosis and oxidative stress, as well as improvement of mitochondrial integrity and biogenesis in post‐MI myocardium.