Abstract

Skeletal muscle myogenesis and injury-induced muscle regeneration contribute to muscle formation and maintenance. As myogenic stem cells, skeletal muscle satellite cells have the ability to proliferate, differentiate and self-renew, and are involved in muscle formation and muscle injury repair. Accumulating evidence suggests that non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), are widely involved in the regulation of gene expression during skeletal muscle myogenesis, and their abnormal expression is associated with a variety of muscle diseases. From the perspective of the molecular mechanism and mode of action of ncRNAs in myogenesis, this review aims to summarize the role of ncRNAs in skeletal muscle satellite cells’ myogenic differentiation and in muscle disease, and systematically analyze the mechanism of ncRNAs in skeletal muscle development. This work will systematically summarize the role of ncRNAs in myogenesis and provide reference targets for the treatment of various muscle diseases, such as muscle dystrophy, atrophy and aberrant hypertrophy.

Highlights

  • As one of the vertebrate striated muscles, skeletal muscle is constituted of myofibers, which have giant multinuclear cells

  • Accumulating evidence suggests that non-coding RNAs, including microRNAs, long non-coding RNAs and circular RNAs, are widely involved in a series of subsequent myogenesis processes such as satellite cell activation, proliferation, differentiation and self-renewal [12,13,14,15] (Tables 1 and 2)

  • This review aims to expand the understanding of skeletal muscle biology and provide reference targets for the treatment of various muscle diseases, such as muscle dystrophy, atrophy, aberrant hypertrophy and cachexia

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Summary

Introduction

As one of the vertebrate striated muscles, skeletal muscle is constituted of myofibers, which have giant multinuclear cells. Whether lncRNA H19 protects the skeletal muscle satellite cells from activation through IGF2-IGF1R signaling remains a mysterious question During both human and mouse satellite cell differentiation, H19 was up-regulated, and down-regulated H19 suppressed satellite cells’ differentiation by reducing the mRNA level of myogenin and MyHC. While the mechanism of the lncRNA Uc.283+A in the quiescence and activation of skeletal muscle satellite cells has not yet been reported, the lncRNA Uc.283+A can rapidly destroy the functional miR-195 by blocking its formation, which is needed to maintain satellite cells’ quiescence, so it may be a potentially key regulator. Recent research has shown that Notch induces the transcription of the quiescence-specific mirtron miR-708, which represses Tensin to inhibit the activation of focal adhesion kinase (FAK), which further stabilizes satellite cells within their niche [58] MiR-34c inhibits the proliferation and promotes the differentiation of porcine muscle satellite cells by inhibiting Notch expression [67]

Inhibits cell proliferation
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