HIF-1α Negatively Regulates Irisin Expression Which Involves in Muscle Atrophy Induced by Hypoxia |
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| Authors: | Shiqiang Liu Pengyu Fu Kaiting Ning Rui Wang Baoqiang Yang Jiahui Chen Huiyun Xu |
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| Affiliation: | 1.Key Laboratory for Space Bioscience and Biotechnology, School of Life Sciences, Northwestern Polytechnical University, Xi’an 710072, China; (S.L.); (K.N.); (R.W.); (B.Y.); (J.C.);2.Department of Physical Education, Northwestern Polytechnical University, Xi’an 710072, China;3.Research Center of Special Environmental Biomechanics & Medical Engineering, Northwestern Polytechnical University, Youyi Xilu 127, Xi’an 710072, China |
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| 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. |
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| Keywords: | hypoxia muscle atrophy HIF-1α irisin FNDC5 |
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