Development and Progression of Alopecia in the Vitamin D Receptor Null Mouse

In this study, researchers found that mice lacking the vitamin D receptor (VDR) gene developed alopecia due to disrupted hair follicle cycling. The hair follicles of Vdr null mice deteriorated during the first catagen phase, failing to cycle normally. This disruption was linked to increased expression of the hairless (Hr) gene, a regulator of hair follicle cycling. Hr levels were higher in Vdr null mice compared to wildtype controls, suggesting that VDR is necessary for regulating Hr expression and normal hair follicle cycling. Both VDR and Hr were essential for maintaining hair follicle structure and function.