Myogenic, genomic and non‐genomic influences of the vitamin D axis in skeletal muscle
Abstract
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 D 3 (1,25[OH] 2 D 3 ) 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) 2 D 3 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) 2 D 3 /VDR.
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