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This study found that women with PCOS had higher levels of Nesfatin-1 and lower levels of vitamin D, which may be linked to increased blood pressure and potential hypertension.

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 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 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.

In this study, Cyanidin 3-O-arabinoside was found to protect against DHT-induced dermal papilla cell senescence and mitochondrial dysfunction in androgenetic alopecia, restoring hair growth in mouse models.

This study indicates that vitamin D3 administration may protect rat hair follicles from radiation-induced damage, as evidenced by maintained follicle numbers and increased Vitamin D receptor activity in treated skin.

This review discusses vitamin D and calcium signaling roles in epidermal stem cell processes essential for wound healing but reports no new experimental results, emphasizing their potential interdependent regulatory mechanisms.

In this study, researchers observed that the absence of the vitamin D receptor or its ligand-activated transcription in mice did not affect glucose homeostasis or gene expression in islets.

This study found that the vitamin D receptor, but not its ligand, regulates genes involved in hair cycle progression, suggesting a role in integrating hormone signaling pathways for hair and epidermal functions.

This study suggests no significant association between vitamin D receptor gene polymorphisms and alopecia areata.

This review discusses inherited forms of vitamin D-dependent rickets and explains their genetic and metabolic causes but reports no new clinical findings.

In this study, researchers observed that the success of treating hereditary vitamin D–resistant rickets in children depends on the mutation location in the VDR gene, notably with favorable dental development outcomes for those with the p.R391S mutation, despite persistent alopecia.

This study characterized two siblings with hereditary vitamin D resistant rickets and a mutation in the vitamin D receptor, finding no immune-related disorders despite a defective T cell response to vitamin D.

This review discusses recent advances in molecular genetics and their impact on the accuracy and understanding of diagnosing inherited skin diseases but reports no new results.

This abstract reports an influenzalike illness with varying antibody titers observed in a woman and her husband, but it does not provide broader clinical findings.

This study found that using conditioned medium from vitamin D3 pre-activated preadipocytes enhanced hair regeneration in mice by promoting angiogenesis.

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 case report observed that while a 4-year-old boy with vitamin D-dependent rickets type II showed biochemical and bone improvement after vitamin D and calcium treatment, his alopecia did not improve.

In this study, researchers found that the vitamin D receptor plays a crucial role in promoting differentiation and protecting against UVB-induced DNA damage in murine melanocytes, suggesting potential implications for melanoma progression.

This case report documents a female toddler with novel compound heterozygous mutations in the VDR gene causing hereditary 1,25-dihydroxyvitamin D-resistant rickets, expanding the known mutation spectrum for this disease.

This study identified three new mutations in the VDR ligand-binding domain that may cause dysfunction, and noted that oral calcium and calcidol treatment was effective, but only one patient experienced hair growth.

This study suggests that the vitamin D receptor and hairless gene may directly regulate each other via a transcriptional mechanism, potentially explaining phenotypic similarities between atrichia and VDRRIIa rickets.

In this study, no significant association was found between the VDR FokI gene polymorphism and alopecia areata, though further research in diverse populations is needed.

This chapter hypothesizes that vitamin D signaling in the skin may suppress UV radiation-induced epidermal tumor formation, reviewing potential mechanisms without reporting new clinical results.

This study demonstrated that mice lacking skin-specific RXRalpha expression developed hair follicle degeneration and alopecia, indicating the importance of RXRalpha/VDR heterodimers in maintaining hair follicle homeostasis.

This study reported a series of eight children with hereditary vitamin D-resistant rickets in Tunisia, identifying both common and novel mutations in the vitamin D receptor gene, and noting significant improvement with intravenous calcium treatment in most patients.

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.

This study identified key lipid differences between black and white hair in individuals with premature greying, highlighting vitamin D3 as a potential target for further research in understanding this condition.

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.

In this study, eight patients with hereditary vitamin D-resistant rickets who share a specific VDR mutation showed improved clinical symptoms except alopecia after up to 11 years of treatment.