Characterization of Type II Rickets Model Rats to Reveal Functions of Vitamin D and Vitamin D Receptor

In this study, researchers observed that Vdr-knockout mice experience hair cycle arrest during the catagen stage, leading to alopecia, with persistent epithelial strands forming in the hair follicles, indicating Vitamin D receptor's role in regulating hair follicle regression and regeneration.

In this study, only Vdr-knockout rats showed both abnormal skin formation and alopecia, which may provide insights into vitamin D receptor function and its role in the hair growth cycle.

This study found that a novel missense mutation in the vitamin D receptor caused hereditary 1,25-dihydroxyvitamin D-resistant rickets with alopecia by disrupting protein function, highlighting the importance of DNA binding in hair development.

This abstract reviews hereditary vitamin D-resistant rickets, a rare genetic condition causing severe early childhood rickets, and reports no new results; effective treatment typically requires high doses of calcium to address hypocalcemia and secondary hyperparathyroidism.

Vitamin D receptor mutations can cause alopecia by affecting hair growth genes.

This study discovered a novel interaction between the vitamin D receptor and LEF1, essential for normal Wnt signaling in keratinocytes, which is crucial for regular hair cycling.

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 research highlights that engineered mice lacking the vitamin D receptor show multiple health issues similar to human vitamin D deficiency, underscoring the widespread impacts of the vitamin D endocrine system.

This study found that the hairless gene product (Hr) suppresses VDR-mediated gene activation by directly interacting with the vitamin D receptor, potentially affecting hair follicle function.

This study found that restoring vitamin D receptor expression specifically in the keratinocytes of VDR null mice prevented alopecia and enhanced hair follicle response during anagen initiation.