Abstract
Skeletal muscle is the most abundant type of tissue in human body, being involved in diverse activities and maintaining a finely tuned metabolic balance. Autophagy, characterized by the autophagosome–lysosome system with the involvement of evolutionarily conserved autophagy-related genes, is an important catabolic process and plays an essential role in energy generation and consumption, as well as substance turnover processes in skeletal muscles. Autophagy in skeletal muscles is finely tuned under the tight regulation of diverse signaling pathways, and the autophagy pathway has cross-talk with other pathways to form feedback loops under physiological conditions and metabolic stress. Altered autophagy activity characterized by either increased formation of autophagosomes or inhibition of lysosome-autophagosome fusion can lead to pathological cascades, and mutations in autophagy genes and deregulation of autophagy pathways have been identified as one of the major causes for a variety of skeleton muscle disorders. The advancement of multi-omics techniques enables further understanding of the molecular and biochemical mechanisms underlying the role of autophagy in skeletal muscle disorders, which may yield novel therapeutic targets for these disorders.
Highlights
Skeletal muscles, a type of highly organized and specialized tissue in vertebrates, make up about 40% of total body mass and play a central role in diverse activities, such as locomotion, macromolecule turnover and storage, energy metabolism, and oxygen consumption (Tortora and Anagnostakos, 1987; Frontera and Ochala, 2015)
These results suggest that a basal level of autophagy is required to degrade misfolding proteins and damaged organelles to maintain homeostasis under normal nutritional conditions, while autophagy is upregulated by AMPK activation to degrade proteins as a source of alternative nutrients and energy under stress responses such as starvation and exercise (Sanchez et al, 2012)
Autophagy inhibition results in muscle atrophy, loss-of-force production, myopathy phenotypes, and loss of muscle mass, which is similar to the phenotypes caused by disrupting the functions of atrogin-1 and MuRF1, two atrophy-related ubiquitin ligases, as well as deficiencies in genes involved in different catabolic pathways (Bodine et al, 2001; Baehr et al, 2011)
Summary
Qianghua Xia1†, Xubo Huang1†, Jieru Huang, Yongfeng Zheng, Michael E. Skeletal muscle is the most abundant type of tissue in human body, being involved in diverse activities and maintaining a finely tuned metabolic balance. Autophagy, characterized by the autophagosome–lysosome system with the involvement of evolutionarily conserved autophagy-related genes, is an important catabolic process and plays an essential role in energy generation and consumption, as well as substance turnover processes in skeletal muscles. Autophagy in skeletal muscles is finely tuned under the tight regulation of diverse signaling pathways, and the autophagy pathway has cross-talk with other pathways to form feedback loops under physiological conditions and metabolic stress. The advancement of multi-omics techniques enables further understanding of the molecular and biochemical mechanisms underlying the role of autophagy in skeletal muscle disorders, which may yield novel therapeutic targets for these disorders.
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