ABSTRACT Vitamin D exerts its biological actions via the vitamin D receptor (VDR). VDR is expressed in many tissues albeit at variable expression. The localization of VDR in myofibers has been confirmed by immunohistochemistry. VDR signaling has been recognized as a potential regulator of myogenesis. Data linking VDR mutations to various muscle phenotypes have been gradually increasing. Genetic animal models accelerate our understanding of the molecular mechanisms by which VDR signaling regulates normal muscle homeostasis. These insights will be valuable in bridging molecular mechanisms and therapeutic strategies for age-related muscle wasting such as sarcopenia. Here, we outline the studies using genetic-modified mice that reveal the role of VDR signaling in muscle structure and function.
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