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Skeletal muscle mitochondrial remodeling in exercise and diseases


Skeletal muscle fitness and plasticity is an important determinant of human health and disease. Mitochondria are essential for maintaining skeletal muscle energy homeostasis by adaptive re-programming to meet the demands imposed by a myriad of physiologic or pathophysiological stresses. Skeletal muscle mitochondrial dysfunction has been implicated in the pathogenesis of many diseases, including muscular dystrophy, atrophy, type 2 diabetes, and aging-related sarcopenia. Notably, exercise counteracts the effects of many chronic diseases on skeletal muscle mitochondrial function. Recent studies have revealed a finely tuned regulatory network that orchestrates skeletal muscle mitochondrial biogenesis and function in response to exercise and in disease states. In addition, increasing evidence suggests that mitochondria also serve to “communicate” with the nucleus and mediate adaptive genomic re-programming. Here we review the current state of knowledge relevant to the dynamic remodeling of skeletal muscle mitochondria in response to exercise and in disease states.

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This work was supported by grants from the National Natural Science Foundation of China (No. 31471110, 31771291); the Ministry of Science and Technology of China (973 Program 2015CB856300); Natural Science Foundation of Jiangsu Province (BK20170014); and Fundamental Research Funds for the Central Universities (090314380023) to Z.G. and NIH grants R01 DK045416, R01 HL058493, and R01 HL128349 to D.P.K.

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The authors declare no competing interests.

Correspondence to Zhenji Gan or Daniel P. Kelly or Rick B. Vega.

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