Despite vitamin D‐deficiency clinically presenting with myopathy, muscle weakness and atrophy, the mechanisms by which vitamin D exerts its homeostatic effects upon skeletal muscle remain to be fully established. Recent studies have shown that the receptor by which 1α,25‐dihydroxyvitamin D₃ (1,25[OH]₂D₃) exerts its biological actions (ie, the vitamin D receptor, VDR) elicits both genomic and non‐genomic effects upon skeletal muscle. The controversy surrounding skeletal muscle VDR mRNA/protein expression in post‐natal muscle has been allayed by myriad recent studies, while dynamic expression of VDR throughout myogenesis, and association of higher VDR levels during muscle regeneration/immature muscle cells, suggests a role in myogenesis and perhaps an enrichment of VDR in satellite cells. Accordingly, in vitro studies have demonstrated 1,25(OH)₂D₃ is anti‐proliferative in myoblasts, yet pro‐differentiation in latter stages of myogenesis. These effects involve modulation of gene expression (VDR as a transcriptional co‐activator controls ~3% of the genome) and post‐genomic intracellular signalling for example, via c‐Src and alterations to intramuscular calcium homeostasis and proteostasis. The aim of this review is to consider the biomolecular role for the vitamin D/VDR axis in myogenesis, while also exploring global evidence for genomic and non‐genomic mechanisms of action for 1,25(OH)₂D₃/VDR.

中文翻译：

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维生素D轴对骨骼肌的肌源性，基因组和非基因组影响

尽管临床上存在维生素D缺乏症，并伴有肌病，肌肉无力和萎缩，但维生素D对骨骼肌发挥稳态作用的机制仍待充分确立。最近的研究表明，该受体通过1α，25-二羟基维生素D ₃（1,25 [OH] ₂ D ₃）发挥其生物学作用（即维生素D受体，VDR）对骨骼肌产生基因组和非基因组作用。近期的大量研究缓解了围绕产后肌肉中骨骼肌VDR mRNA /蛋白质表达的争议，而在整个肌肉形成过程中VDR的动态表达以及肌肉再生/未成熟肌肉细胞中较高VDR水平的关联表明在肌肉形成中的作用以及卫星细胞中VDR的丰富化。因此，体外研究表明1,25（OH）₂ D ₃在成肌细胞中具有抗增殖作用，而在成肌后期则具有促分化作用。这些作用包括调节基因表达（VDR作为转录共激活因子控制约3％的基因组）和基因组后细胞内信号转导，例如通过c-Src以及肌内钙动态平衡和蛋白稳态的改变。这篇综述的目的是考虑维生素D / VDR轴在肌发生中的生物分子作用，同时也探索有关1,25（OH）₂ D ₃ / VDR作用的基因组和非基因组作用机理的全球证据。