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This study found that CYP11A1-derived vitamin D3 analogs inhibit fibroblast proliferation and decrease collagen production through VDR expression, showing potential antifibrotic and antiproliferative activity in human dermal fibroblasts.

In this study, a Chinese Han family with hereditary vitamin D-resistant rickets was found to have a homozygous missense mutation in the VDR gene, and the affected individual uniquely responded well to treatment with oral calcium and low-dose calcitriol.

This study found that a novel R343H mutation in the vitamin D receptor gene impairs its transcription activity, contributing to hereditary vitamin D-resistant rickets and alopecia in the affected family.

This study found that mice lacking REDD1 experienced an expansion of dermal white adipose tissue through both hypertrophy and hyperplasia, suggesting a potential therapeutic target for skin adipogenesis regulation.

This study highlights the complex role of the vitamin D receptor in skin processes, where its disruption, along with calcium and co-regulator imbalances, could contribute to skin cancer development by altering skin differentiation and hair follicle cycling.

This minireview discusses a proposed model of the vitamin D receptor that explains how 1alpha,25(OH)2D3 can mediate both genomic and rapid responses through different ligand shapes and cellular locations, without presenting new research findings.

This study describes a patient with hereditary vitamin D resistant rickets (HVDRR) who, despite having a truncated vitamin D receptor, did not exhibit typical hair or skin abnormalities, suggesting possible compensation via interactions with other proteins.

This study found that vitamin D deficiency in patients with alopecia areata was associated with greater disease severity and longer duration, but not with disease pattern or vitamin D receptor expression.

This study found that the vitamin D receptor, but not its ligand, regulates genes involved in hair cycle progression, suggesting a role in integrating hormone signaling pathways for hair and epidermal functions.

This study suggests that the vitamin D receptor and hairless gene may directly regulate each other via a transcriptional mechanism, potentially explaining phenotypic similarities between atrichia and VDRRIIa rickets.

This review summarizes the proposed model that describes how different shapes of 1alpha,25(OH)2D3 ligands interact with the vitamin D receptor to mediate genomic and rapid responses in cells.

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.

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 identified new dietary ligands for the human vitamin D receptor, including curcumin and gamma-tocotrienol, which may influence its biological functions.

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 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 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 study found that the vitamin D receptor is crucial for initiating the postnatal hair follicular cycle in mice, preventing alopecia associated with its inactivation.

This study found that the protein hairless acts as both a corepressor and coactivator of the vitamin D receptor, influencing gene transcription in a ligand-selective manner.

This study indicates that vitamin D3 administration may protect rat hair follicles from radiation-induced damage, as evidenced by maintained follicle numbers and increased Vitamin D receptor activity in treated skin.

In this study, eight patients with hereditary vitamin D-resistant rickets who share a specific VDR mutation showed improved clinical symptoms except alopecia after up to 11 years of treatment.

This review discusses the role of various hormones in diffuse hair loss and emphasizes the need for further research to clarify their complex interactions and potential therapeutic implications, but reports 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 review discusses the regulation and function of vitamin D and its receptor in skin cells, highlighting their roles in processes such as proliferation inhibition, differentiation, and innate immunity, but reports no new results.

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 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 identified the Hairless (Hr) gene-encoded protein as a corepressor that plays a crucial role in maintaining skin and hair by regulating epithelial stem cell differentiation and gene expression via chromatin remodeling, which may impact both development and disease.

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.