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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 specific polymorphisms in the VDR gene, Taq1, and Cdx1, were significantly associated with increased risk of chronic telogen effluvium in women.

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 study found that vitamin C deficiency in SMP-30/GNL-KO mice affected gene expression related to hair growth and cell growth, resulting in delayed hair growth compared to those with adequate vitamin C.

In this study, researchers observed that the absence of a functional vitamin D receptor in mice leads to impaired hair follicle regeneration due to defects in keratinocyte stem cells, resulting in alopecia.

This study suggests that while VDR is crucial for maintaining hair follicles in mice, their degeneration may be linked to impaired cell migration during hair growth phases rather than stem cell loss.

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 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.

Vitamin D receptor mutations can cause alopecia by affecting hair growth genes.

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

This study found that the vitamin D receptor plays a crucial role in hair follicle development in cashmere goats by regulating signaling pathways in dermal papilla cells.

This review discusses the role of vitamin D receptor signaling in hair follicle biology for alopecia treatment and underscores the need for continued research, without presenting new clinical 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 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 hair follicle homeostasis in mice requires vitamin D receptor expression in keratinocytes, independent of its ligand activation.

This study found that the hairless gene product (Hr) suppresses VDR-mediated gene activation by directly interacting with the vitamin D receptor, potentially affecting hair follicle function.

This study found that absence of the vitamin D receptor in keratinocytes impairs canonical Wnt signaling and leads to alopecia due to defects in keratinocyte stem cells.

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 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 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 study found that vitamin D receptor expression is associated with proliferating keratinocytes, while retinoid X receptor α is linked to differentiating keratinocytes, suggesting differential targeting by vitamin D metabolites.

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 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 their mouse study, Oda et al. found that removing the MED1 gene in the skin led to hair loss and changes in epidermal cell differentiation, indicating MED1's significant role in these processes.

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, 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 case report describes a patient with mutations in both alleles of the vitamin D receptor who exhibited hair loss clinically indistinguishable from generalized atrichia with papules, suggesting a potential genetic pathway shared with the hairless gene.

This study observed that the vitamin D receptor is crucial for hair follicle formation and altering tumor development in the Wnt signaling pathway, suggesting therapeutic potential for vitamin D analogues in related tumors.

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.