期刊
BIOMEDICINES
卷 9, 期 6, 页码 -出版社
MDPI
DOI: 10.3390/biomedicines9060701
关键词
exercise training; myocardial infarction; mice; mitophagy; irisin
资金
- National Natural Science Foundation of China [31671240, 31900828]
Different types of exercise and skeletal muscle electrical stimulation can up-regulate the expression of irisin/FNDC5 in the myocardium, promoting mitophagy and improving cardiac function. Resistance exercise can improve cardiac function by activating the irisin/FNDC5-PINK1/Parkin-LC3/P62 pathway and inhibiting oxidative stress.
Myocardial infarction is the major cause of death in cardiovascular disease. In vitro and in vivo models are used to find the exercise mode which has the most significant effect on myocardial irisin/FNDC5 expression and illuminate the cardioprotective role and mechanisms of exercise-activated myocardial irisin/FNDC5-PINK1/Parkin-mediated mitophagy in myocardial infarction. The results indicated that expression of irisin/FNDC5 in myocardium could be up-regulated by different types of exercise and skeletal muscle electrical stimulation, which then promotes mitophagy and improves cardiac function and the effect of resistance exercise. Resistance exercise can improve cardiac function by activating the irisin/FNDC5-PINK1/Parkin-LC3/P62 pathway, regulating mitophagy and inhibiting oxidative stress. OPA1 may play an important role in the improvement of cardiac function and mitophagy pathway in myocardial infarction mice by irisin-mediated resistance exercise. Resistance exercise is expected to become an effective therapeutic way to promote myocardial infarction rehabilitation.
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