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The study found that normalizing mineral ion levels in vitamin D receptor-ablated mice prevented hyperparathyroidism and bone disorders but did not address hair loss, indicating the VDR's role in hair growth.

This study found that normalizing mineral ion levels in vitamin D receptor-ablated mice prevented hyperparathyroidism, rickets, and osteomalacia, but alopecia persisted, indicating a separate role for the receptor in hair growth.

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 unliganded vitamin D receptors in mice may cause more severe skeletal and mineral ion defects than VDR-null conditions, and vitamin D analogues may restore function in specific VDR mutations.

This study found that preventing abnormal mineral ion homeostasis in vitamin D receptor knockout mice stopped bone abnormalities, while the animal's skin phenotype arose from direct receptor effects independent of vitamin D.