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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.

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 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.

In this study, the researchers found that alopecia in VDR null mice is likely due to issues with hair cycle initiation rather than defects in keratinocyte proliferation or differentiation.

This study suggests that alopecia in vitamin D receptor null mice is due to impaired initiation of the hair cycle rather than defects in keratinocyte proliferation or differentiation.

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

This review discusses the molecular role of the vitamin D receptor in regulating various biological actions such as bone mineralization and reports no new clinical results, highlighting the complexity of vitamin D's function in multiple tissues.

This research suggests that the vitamin D receptor may regulate hair follicle cycling and provide genoprotection against skin carcinogenesis through a mechanism independent of 1,25-dihydroxyvitamin D3, based on evidence from mouse models.

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 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.

This study observed that 25-hydroxyvitamin D3 restored rickets symptoms in genetically modified rats, suggesting its direct action through vitamin D receptor pathways.

This study found that deleting β-catenin in epidermis-specific VDR knockout mice did not prevent UVB-induced skin tumors, indicating β-catenin does not compensate for VDR's role in tumor suppression.

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.

This study observed that vitamin D receptor knockout mice exhibit impaired epidermal differentiation and progressive hair loss, suggesting the importance of the vitamin D receptor in normal skin and hair follicle development.

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 study found that preventing abnormal mineral ion homeostasis in vitamin D receptor knockout mice stopped bone abnormalities, while the animal's skin phenotype arose from direct receptor effects independent of vitamin D.

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.

This study observed that knocking out the 1α-hydroxylase gene in mice resulted in rickets and growth retardation, demonstrating the enzyme's crucial role in vitamin D function in animals.

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.

This study found that the vitamin D receptor is essential for the self-renewal, migration, and differentiation of epidermal stem cells during skin wound healing in mice.

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 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.

In this study, gene therapy using a VDR-expressing adenoviral vector significantly improved hair growth and reduced cyst formation in Vdr -KO rats with alopecia linked to type II rickets, whereas control treatments did not show these effects.

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 study suggests that lithocholic acid may enhance hair regeneration in alopecia by activating vitamin D receptors in human dermal papilla cells.

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 found that RXRα plays a critical role in hair cycling and keratinocyte functions in mice, likely through its interaction with VDR in epidermal cells.

This study found that ΔNp63α directly regulates VDR expression, which in turn may reduce invasiveness in an epidermoid cancer cell line.