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This review examines the functions of vitamin D and its receptor in skin and explores how these are regulated, reporting no new clinical results.

This review examines the impact of vitamin D signaling in extraskeletal tissues and notes that expected benefits from animal and cell studies have not been consistently replicated in human clinical trials.

This study found that the vitamin D receptor in lampreys, which lack bones and hair, binds 1,25-dihydroxyvitamin D3 and may function to induce enzymes for detoxifying substances.

This study found that the absence of the vitamin D receptor disrupts hair follicle structure during the first catagen in mice, linked to increased expression of the hairless gene.

This review examines the role of Hairless, a nuclear receptor corepressor, in regulating Wnt signaling during hair cycling and reports no new clinical results.

This review examines the role of nuclear hormone receptors in skin wound repair processes and reports no new clinical results, highlighting the importance of their interaction with skin cells for effective healing.

This review discusses hormonal influences on hair growth and suggests that understanding hormone-gene interactions may improve treatment of hirsutism and alopecia, but reports no new clinical findings.

This study found that humanized mouse models expressing mutated or reduced levels of the vitamin D receptor were able to maintain normal mineral homeostasis and prevent typical symptoms of vitamin D resistance.

This study created a humanized mouse model of hereditary vitamin D-resistant rickets that lacks alopecia, indicating the mutant receptor's potential to explore the syndrome's characteristics beyond vitamin D binding.

This study suggests that lower serum and tissue vitamin D receptor levels in alopecia areata and androgenetic alopecia patients may play a role in the pathogenesis of these hair diseases.

This study identified two distinct VDR gene mutations among Lebanese families with hereditary vitamin D-resistant rickets, noting varied treatment responses and promising outcomes despite severe phenotypes.

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.

In this study, homozygous VDR null mutant mice exhibited nonfunctional vitamin D receptors, leading to growth abnormalities and revealing the limited physiological importance of vitamin D pathways outside the classical receptor.

This study found that absence of the vitamin D receptor in keratinocytes impairs canonical Wnt signaling and leads to alopecia due to defects in keratinocyte stem cells.

This research suggests that the vitamin D receptor may regulate hair follicle cycling and provide genoprotection against skin carcinogenesis through a mechanism independent of 1,25-dihydroxyvitamin D3, based on evidence from mouse models.

This study identified complex regulatory elements and interactions involving the Hr gene and HR protein that are crucial for hair follicle formation and cycling in mammals.

This study identified a novel V26M mutation in the vitamin D receptor as the cause of hereditary vitamin D resistant rickets in a patient, characterized by severe rickets and an unusual pattern of alopecia.

In this study, researchers observed that the absence of a functional vitamin D receptor in mice leads to impaired hair follicle regeneration due to defects in keratinocyte stem cells, resulting in alopecia.

This chapter discusses the molecular biology of the vitamin D receptor in gene transcription and reports no new results; it highlights recent findings on receptor activity independent of its usual ligand.

This article compares two rare genetic diseases, vitamin D-dependent rickets type 1 and type 2, focusing on their similar presentations of hypocalcemia and rickets in infancy, but reports no new clinical results.

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.

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 case report describes a patient with mutations in both alleles of the vitamin D receptor who exhibited hair loss clinically indistinguishable from generalized atrichia with papules, suggesting a potential genetic pathway shared with the hairless gene.

This study observed that the vitamin D receptor is crucial for hair follicle formation and altering tumor development in the Wnt signaling pathway, suggesting therapeutic potential for vitamin D analogues in related tumors.

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 article reviews the role of vitamin D receptor in protecting the skin from UV radiation-induced damage and tumor formation, but it reports no new clinical results.

A genetic mutation caused severe rickets and alopecia in an Indian patient, but high-dose calcium and phosphate treatment improved their condition.

This study found that vitamin D receptor expression is associated with proliferating keratinocytes, while retinoid X receptor α is linked to differentiating keratinocytes, suggesting differential targeting by vitamin D metabolites.

In this study, researchers observed that the success of treating hereditary vitamin D–resistant rickets in children depends on the mutation location in the VDR gene, notably with favorable dental development outcomes for those with the p.R391S mutation, despite persistent alopecia.

This review discusses the role of the unliganded vitamin D receptor in hair follicle cycling and tumor formation in mice and reports no new experimental findings.