Abstract
Skeletal muscle atrophy, a conventional clinical feature in patients with cancer, chronic obstructive pulmonary disease, sepsis and severe burns, is defined as a reduction in muscle mass. During atrophy, the protein degradation is abnormally activated and the aberrance between protein synthesis and protein degradation results in muscle atrophy. Previous studies have demonstrated that miRNAs, small non-coding RNA molecules, serve an important role in the regulation of muscle atrophy. Further studies have indicated the implications of the ubiquitin-proteasome and PI3K/Akt/FoxO signaling pathways and myogenic regulatory factors in miRNA-mediated muscle atrophy. Therefore, in this review, the effects and molecular mechanisms of miRNAs on muscle atrophy are summarized, leading to the suggestion that miRNAs may serve as potential therapeutic targets in muscle atrophy.
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