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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 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 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 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 applied to mouse skin caused more wrinkles and sagging due to changes in the skin's outer layer.

This report describes siblings with vitamin D-dependent rickets type 2, characterized by growth retardation, alopecia totalis, and low 25(OH)D3 levels, highlighting its autosomal recessive pattern and distinction from other rickets types.

Vitamin D3 affects cell differentiation in specific skin areas.

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.

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 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 obese Egyptian women with polycystic ovary syndrome had significantly lower serum 25-OH vitamin D levels compared to non-obese women with the condition.

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

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 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, 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 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 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.

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

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.

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 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 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 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 case study reports that a 3 ½ year-old male with vitamin D-dependent type II rickets showed partial improvement in alopecia and rickets when treated with high doses of 1,25(OH)2 vitamin D3.

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 highlights the crucial role of vitamin D signaling in epidermal stem cells during skin wound healing, emphasizing its distinct functions from calcium metabolism and its importance in genomic regulation mediated by the vitamin D receptor.

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.

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 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 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.