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This study found that 1,25-dihydroxyvitamin D3 promotes hair growth and regeneration in mice by prolonging the anagen phase and counteracting DHT's inhibitory effects, suggesting its potential therapeutic role for androgenetic alopecia.

This study found that after topical application in rats, 1,24-dihydroxyvitamin D3 absorbed through both the stratum corneum and hair follicles, with about 30% excreted via the faeces.

In this study, researchers identified a unique Arg30stop mutation in the vitamin D receptor gene that causes hereditary vitamin D-resistant rickets in a young French-Canadian boy by truncating the receptor and causing hormone resistance.

This study found that in a mouse model with hereditary 1,25-dihydroxyvitamin D resistant rickets, a mutant vitamin D receptor lacking hormone-binding ability could restore normal hair cycling and affect parathyroid hormone regulation.

This study identified a novel nonsense mutation in the VDR gene in two patients with hereditary vitamin D resistant rickets and alopecia, leading to resistance to 1,25-dihydroxyvitamin D3.

This study found that vitamin D receptor activation in primary keratinocytes can occur independently of the 1,25-dihydroxyvitamin D₃ ligand, likely through interaction with retinoid X receptors.

Vitamin D3 affects cell differentiation in specific skin areas.

This study found that human keratinocytes' sensitivity and response to vitamin D3 analogues vary based on cell density, serum availability, and calcium concentration.

This report describes two sisters with rickets and alopecia unresponsive to high doses of vitamin D2, where oral phosphorus supplements led to significant clinical improvement.

This study found that mice lacking the vitamin D receptor (VDR) developed skin tumors more rapidly than those with normal VDR activity, regardless of 1,25-dihydroxyvitamin D(3) presence.

This study found that measuring 24-OHase induction by 1,25(OH)2D3 in cultured skin fibroblasts is a sensitive test for detecting genetic defects in the 1,25(OH)2D effector pathway.

This study suggests that vitamin D and its receptor may protect against the development of epidermal tumors following UV radiation by regulating specific cellular signaling pathways.

This study reported a case of hereditary vitamin D–resistant rickets caused by a single heterozygous missense mutation in the VDR gene, showing dominant-negative effects and reduced response to 1,25-dihydroxyvitamin D3.

This article reviews the multifaceted roles of vitamin D beyond bone health and notes its potential involvement in reducing risks of certain cancers and autoimmune diseases, but it presents no new clinical results.

This study found that VDR deficiency in mice leads to various skin pathologies but does not affect the phenotype or function of Langerhans cells.

This study characterized two siblings with hereditary vitamin D resistant rickets and a mutation in the vitamin D receptor, finding no immune-related disorders despite a defective T cell response to vitamin D.

Vitamin D3 may prevent hair loss from chemotherapy, but side effects and cancer cell protection are concerns.

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 reports that the epidermis is both a source and target for vitamin D3's active form, influencing skin and hair follicle differentiation through a calcium-mediated pathway.

This case report details a severe instance of VDR-II where intravenous calcium infusions, administered nightly, successfully improved clinical, radiological, and biochemical signs of rickets without alopecia despite ineffective calcitriol therapy.

This study found that the vitamin D-VDR system is crucial for mineral and bone metabolism post-weaning and identified missense mutations in 1alpha-hydroxylase causing type I rickets.

This study found that relatively low concentrations of 1,25(OH)2D3 stimulated human hair follicle and fiber growth, while higher concentrations inhibited growth in a whole-organ culture system.

In this study, distinct clinical responses and long-term resistances were observed in two pediatric patients with vitamin D-dependency type II, associated with abnormalities in their skin fibroblast interactions with 1,25-(OH)2D3.

This case study describes a child with rickets and alopecia who responded to a small dose of 1-a-hydroxyvitamin D3, but her alopecia remained unchanged despite treatment.

This study found that alopecia in hereditary resistance to 1,25(OH)2D may indicate a more severe form of the condition, associated with earlier diagnosis and different responses to calciferol therapy.

This report describes a unique case of hereditary vitamin D-resistant rickets (HVDRR) in a dog, caused by a VDR gene mutation resulting in severe hypocalcemia and bone issues, which presented with symptoms similar to those observed in humans.

In this mouse study, topical 1,25-dihydroxyvitamin D3 protected against cyclophosphamide-induced hair loss and inhibited mammary tumor growth, with effects varying by sex and tumor presence.

This study found that both the natural ligand 1alpha,25(OH)(2)D(3) and the synthetic agonist LG190178 bind similarly to the vitamin D receptor's coregulator motifs, suggesting similar biological functions.

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.

This article reviews the essential role of vitamin D in bone health and its various clinical applications but reports no new clinical findings.