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This study found that mice lacking the Vitamin D receptor showed disrupted hair follicle cycling, which was partially restored with hedgehog signaling pathway activation, suggesting a role for this pathway in follicle regulation independent of vitamin D.

This study observed that Cyp27b1−/− mice exhibited growth and skeletal abnormalities similar to those of Vdr−/− mice, despite differences like the development of alopecia in Vdr−/− mice, suggesting that 1α,25D3 may directly influence chondrocyte proliferation and differentiation.

In this study, the researchers found that alopecia in VDR null mice is likely due to issues with hair cycle initiation rather than defects in keratinocyte proliferation or differentiation.

This study suggests that alopecia in vitamin D receptor null mice is due to impaired initiation of the hair cycle rather than defects in keratinocyte proliferation or differentiation.

This study found that VDR knockout mice exhibited muscle and motor impairments affecting locomotor behavior, while cognitive functions such as exploration, working memory, and anxiety appeared unaffected.