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This study found that mice lacking the Vitamin D receptor showed disrupted hair follicle cycling, which was partially restored with hedgehog signaling pathway activation, suggesting a role for this pathway in follicle regulation independent of vitamin D.

In this study, researchers found that the "U" allele of the Tru9I variant may be associated with low vitamin D levels and altered VDR gene activity in alopecia areata patients, while the "u" allele might have a protective role against developing the condition.

This study found that CRP levels were elevated in alopecia areata patients, with an inverse linear association between serum vitamin D and CRP levels specifically noted in ophiasis AA.

This study found that normalizing mineral ion levels in vitamin D receptor-ablated mice prevented hyperparathyroidism, rickets, and osteomalacia, but alopecia persisted, indicating a separate role for the receptor in hair growth.

This study showed that vitamin D receptor gene-deficient rats exhibit hair loss and skin abnormalities due to differences in gene and protein expression patterns, while ligand-independent VDR action is crucial for normal hair cycle maintenance and skin formation.

This study described the clinical and genetic features of two Iranian siblings with hereditary vitamin D resistant rickets, identifying a specific VDR gene mutation contributing to their symptoms.

In this case report, a four-year-old girl was diagnosed with vitamin D-dependent rickets type II, manifesting as diffuse alopecia, frontal bossing, hypoplastic teeth, and skin-colored papules, due to a genetic mutation causing resistance to 1.25-dihydroxy vitamin D.

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 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 review highlights the potential role of vitamin D and its analogs in managing alopecia areata, noting that vitamin D deficiency and altered receptor expression may be linked to disease severity and that supplementation could help reduce severity and relapse rates.

This study found that VDR deficiency in mice leads to various skin pathologies but does not affect the phenotype or function of Langerhans cells.

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 observed that Cyp27b1−/− mice exhibited growth and skeletal abnormalities similar to those of Vdr−/− mice, despite differences like the development of alopecia in Vdr−/− mice, suggesting that 1α,25D3 may directly influence chondrocyte proliferation and differentiation.

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.

This study suggests that vitamin D and calcium signaling are crucial for normal wound healing, with deficiencies in these pathways potentially delaying recovery due to diminished stem cell activity and response.

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.

The study found that normalizing mineral ion levels in vitamin D receptor-ablated mice prevented hyperparathyroidism and bone disorders but did not address hair loss, indicating the VDR's role in hair growth.

In this study, the researchers found that vitamin D and calcium signaling in keratinocytes are essential for normal skin regeneration after wounding, with deficiencies significantly delaying wound closure and re-epithelialization in mice.

This review discusses how vitamin D and calcium signaling are essential for wound healing by activating epidermal and hair follicle stem cells, noting that deficiencies may lead to delayed or chronic wounds.

This study found that a hypomorphic mutation in the Hr gene contributes to the development of diet-induced pruritic atopic skin in mice, particularly when combined with dietary deficiencies of polyunsaturated fatty acids and starch.

This study found that alopecia in VDR-null mice persists despite undetectable vitamin D levels, indicating a defect in epithelial-mesenchymal communication due to the absence of ligand-independent receptor function.

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 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 vitamin D receptor signaling in mice impairs the inflammatory response to skin injury, particularly affecting macrophage recruitment and granulation tissue formation.

In this study, gene therapy using a VDR-expressing adenoviral vector promoted hair growth in Vdr-KO rats, suggesting its potential for treating alopecia associated with type II rickets.

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 mice lacking both vitamin D and calcium-sensing receptors in epidermal keratinocytes are predisposed to developing squamous cell carcinoma as they age, due to impaired oxidative stress response and reduced DNA repair capabilities.

Vitamin D receptor is crucial for hair growth, not vitamin D itself.

This study found that mice lacking the vitamin D receptor showed disrupted hair follicle cycling and balance between cell proliferation and differentiation, highlighting VDR's role in hair cycling regulation.

This study found that vitamin D and calcium signaling are essential for effective wound repair by maintaining and activating stem cells and aiding in their migration and differentiation.