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This study found that DVd therapy is at least as effective as VAD/VAd for treating multiple myeloma and causes fewer side effects and reduced hospital visits.

In this case study, a girl with hereditary vitamin D resistant rickets had a novel mutation in the VDR gene that affected hair cycling without causing total alopecia, suggesting ligand-independent VDR function in hair cycling.

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 suggests that impaired VDR signaling in mice leads to dysregulated Ddit4 expression, impacting hair cycle progression and wound healing.

This study found that the rs2228570 polymorphism of the VDR gene was associated with an increased risk of melanoma, while the rs731236 polymorphism was linked to a protective effect against the disease in Colombian patients.

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.

In this study, researchers observed that Vdr-knockout mice experience hair cycle arrest during the catagen stage, leading to alopecia, with persistent epithelial strands forming in the hair follicles, indicating Vitamin D receptor's role in regulating hair follicle regression and regeneration.

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 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.

Nutrition plays a key role in managing skin disorders, with specific dietary changes helping improve conditions like acne, dermatitis, psoriasis, alopecia, and skin cancer.

In this study involving genetically modified rats, researchers observed that specific mutations in the vitamin D receptor affect calcium levels and bone formation, emphasizing the receptor's role in maintaining healthy bone density and its importance in regulating hair cycle and skin health.

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 case report describes a rare instance of Vogt-Koyanagi-Harada disease in a 21-year-old Asian woman, highlighting unusual oral manifestations such as tooth discoloration and misalignment, which expand the known clinical spectrum of the disorder.

This study observed that Vitamin D receptor expression at protein and mRNA levels was significantly lower in the hair follicles of alopecia areata patients compared to healthy individuals.

In this study, only Vdr-knockout rats showed both abnormal skin formation and alopecia, which may provide insights into vitamin D receptor function and its role in the hair growth cycle.

In this case report, a 25-year-old woman with VKHD experienced an unusual occurrence of vellus-like hair growth on her normally hairless palm, observed twice over two years, expanding the known integumentary manifestations of VKHD.

This study found that VDR knockout mice exhibited muscle and motor impairments affecting locomotor behavior, while cognitive functions such as exploration, working memory, and anxiety appeared unaffected.

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.

Versican in dermal papilla cells is crucial for healthy hair growth.

This study found that VDAC2 promotes apoptosis in secondary hair follicle stem cells of Albas cashmere goats by activating the P53 signaling pathway, with knockdown of VDAC2 reducing apoptosis and a P53 inhibitor partially rescuing VDAC2-induced apoptosis.

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 in Vdr-knockout mice, hair follicles fail to complete the catagen stage, leading to persistent epithelial strands and subsequent hair loss.

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 review discusses the multifaceted role of vitamin D in the body, noting its influence on calcium balance, hair cycle maintenance, cell proliferation, cardiovascular function, and immune modulation, with no new clinical results reported.

This review explores the potential impact of nutrition on immune-mediated inflammatory skin diseases and evaluates whether dietary changes could help in treatment planning, but it presents no new clinical outcomes.

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 cubosomes combined with dissolving microneedles enhanced transdermal penetration and hair growth efficacy of beta-sitosterol for treating alopecia.

This study observed that vitamin D therapy may help manage alopecia areata, totalis, and universalis, with promising hair regrowth in some pediatric cases, though further trials are needed.

In this study, a novel VDR gene mutation was identified in a child with HVDRR, and the researchers observed that high-dose intravenous calcium therapy led to significant and sustained improvement in rickets symptoms.

In this study, researchers identified a novel p.R50X mutation in the vitamin D receptor gene, linked to hereditary vitamin D-resistant rickets in two siblings.