Abstract
Exposure to high altitude environment leads to skeletal muscle atrophy. As a hormone secreted by skeletal muscles after exercise, irisin contributes to promoting muscle regeneration and ameliorating skeletal muscle atrophy, but its role in hypoxia-induced skeletal muscle atrophy is still unclear. Our results showed that 4 w of hypoxia exposure significantly reduced body weight and gastrocnemius muscle mass of mice, as well as grip strength and the duration time of treadmill exercise. Hypoxic treatment increased HIF-1α expression and decreased both the circulation level of irisin and its precursor protein FNDC5 expression in skeletal muscle. In in vitro, CoCl2-induced chemical hypoxia and 1% O2 ambient hypoxia both reduced FNDC5, along with the increase in HIF-1α. Moreover, the decline in the area and diameter of myotubes caused by hypoxia were rescued by inhibiting HIF-1α via YC-1. Collectively, our research indicated that FNDC5/irisin was negatively regulated by HIF-1α and could participate in the regulation of muscle atrophy caused by hypoxia.
Highlights
Academic Editor: Nam Deuk KimSkeletal muscles account for more than 40% of the body and are responsible for converting chemical energy into mechanical energy to generate force and power, maintain posture, and produce movement [1]
We investigated the role of fibronectin type III domain-containing protein 5 (FNDC5)/irisin in muscle atrophy caused by hyhypoxia in vivo and in vitro and identified that the decreased expression of FNDC5/irisin poxia in vivo and in vitro and identified that the decreased expression of FNDC5/irisin and and the myogenic factors myogenic regulatory factor 4 (Mrf4) and MyoG may be important reasons in hypoxia-induced the myogenic factors Mrf4 and MyoG may be important reasons in hypoxia-induced muscle muscle atrophy
We found that irisin expression washypoxia negatively regulatedreduced by hypoxia-induced factor-1 α (HIF-1α), area
Summary
Skeletal muscles account for more than 40% of the body and are responsible for converting chemical energy into mechanical energy to generate force and power, maintain posture, and produce movement [1]. Studies have reported that ambient hypoxia in the high-altitude region can be the main reason for skeletal muscle atrophy, the mechanism is still unclear. The expression trend of FNDC5/irisin was consistent with MyoG muscle human atrophy.myotubes. Previous studies have found that hypoxia poxia inhibits irisin expression in cardiomyocytes [18] and serum of volunteers who parinhibits irisin in cardiomyocytes [18] and of volunteers participated ticipated in theexpression. We investigated the role of FNDC5/irisin in muscle atrophy caused by. We found that the expression of FNDC5/irisin was negatively regulated by lated by HIF-1α in hypoxia
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