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This study found that mice lacking the 1αOHase enzyme, which is responsible for producing a key vitamin D metabolite, showed impaired epidermal differentiation and delayed recovery of skin barrier function after disruption.

This study found that transfecting keratinocytes with the 1α-OHase gene enhances local production of 1α,25-dihydroxyvitamin D3, suggesting a potential new therapy for skin conditions like psoriasis without causing hypercalcemia or resistance.

In this study, mutations in the vitamin D receptor were identified in Brazilian children with rickets and alopecia, leading to impaired receptor activation and reduced 24-hydroxylase expression.

This study found that 1,25 dihydroxyvitamin D3 significantly increased the expression and activity of vasculoprotective natriuretic peptide receptor-A in cultured inner medullary collecting duct cells, suggesting a potential mechanistic role in cardiovascular and renal benefits.

This study observed wide clinical diversity among five patients with the same VDR gene mutation causing vitamin D-dependent rickets type II, suggesting involvement of a nuclear accessory factor and a nongenomic action of the vitamin.