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In this study, patients with alopecia areata were found to have significantly lower serum vitamin D levels compared to those with vitiligo and healthy individuals, with lower levels correlating with increased disease severity.

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.

Lack of vitamin D receptor increases skin tumor risk by boosting hedgehog signaling.

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 article outlines the potential for upregulating the vitamin D receptor in treating hair disorders, emphasizing the need for further studies to evaluate vitamin D's role in the hair cycle.

This study suggests that there is a U-shaped relationship between vitamin D hormonal forms and aging, with an optimal serum calcidiol concentration needed to minimize aging-related chronic disease risk.

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 study suggests that vitamin D and calcium signaling play a crucial role in wound healing by regulating stem cell activation through enhanced β-catenin transcriptional activity in mice.

This study describes a case of vitamin D resistant rickets in a young girl due to end organ unresponsiveness, highlighting a possible new subtype of the disorder with distinct clinical features.

This case study describes a child with an unusual form of vitamin D-dependent rickets, characterized by alopecia and a deficient response to active vitamin D.

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 study found that Hairless (Hr) acts as a corepressor of the vitamin D receptor (VDR) in human keratinocytes, blocking the action of vitamin D on keratinocyte differentiation.

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 study found that PDGF-D acts as a potent mitogenic factor in adipose-derived stem cells, enhancing their proliferation, migration, and growth factor expression, suggesting its use as a preconditioning agent for ASC transplantation.

This study identified a novel I268T mutation in the vitamin D receptor that reduces its function, contributing to hereditary vitamin D-resistant rickets, and found that a potent vitamin D analog could improve receptor function.

This study found that low serum ferritin and vitamin D2 levels are associated with hair loss in females with chronic telogen effluvium and female pattern hair loss, suggesting potential benefits of screening and supplementation.

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 AR/VDR-targeted agonist hormone therapy can inhibit cell viability in HR2-av triple-negative breast cancer cell lines through multiple mechanisms and may enhance the effects of chemotherapy.

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 abstract discusses two types of hereditary vitamin D metabolism defects, VDDR I and VDDR II, and reports on their distinct characteristics and treatment responses, without presenting new clinical data.

This study found that the absence of unliganded vitamin D receptor significantly impairs cWnt and hedgehog signaling pathways necessary for hair cycle initiation in VDR-null mice.

This study found that the absence of vitamin D receptor signaling in mice impairs the inflammatory response to skin injury, particularly affecting macrophage recruitment and granulation tissue formation.

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 found significantly lower serum vitamin D concentrations in patients with alopecia areata compared to healthy controls, suggesting that vitamin D deficiency may be a risk factor for this autoimmune hair loss disease.

This study found that hair follicle homeostasis in mice requires vitamin D receptor expression in keratinocytes, independent of its ligand activation.

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.

This study found that while calcium can substitute for the Vitamin D receptor in maintaining epidermal keratinocyte differentiation, it cannot compensate for hair follicle dysfunction caused by the absence of the receptor.

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.

This case study reported that absence of alopecia does not reliably predict responsiveness to vitamin D treatment in Vitamin D-dependent rickets type II, as demonstrated by a patient with normal hair growth who showed extreme resistance.