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Vitamin D3 may prevent hair loss from chemotherapy, but side effects and cancer cell protection are concerns.

This review examines the functions of vitamin D and its receptor in skin and explores how these are regulated, reporting no new clinical results.

Vitamin D3 and its receptor are important for hair growth, and understanding receptors could help treat hair graying and skin cancer.

This study found that ablating cyclin D3 in a Ras-dependent skin carcinogenesis model increased apoptosis in hair follicles, reducing papilloma development but potentially facilitating malignant progression when CDK6 is overexpressed.

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.

In a case study of vitamin D-dependent rickets type 2A, researchers observed that while active vitamin D treatment failed to improve bone and laboratory abnormalities, oral calcium lactate significantly ameliorated these issues, although skin and hair problems remained unresponsive.

This study found that most pathogenic HR mutants associated with atrichia with papular lesions had abolished corepressor activity due to defective interactions with histone deacetylases.

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.

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.

This study found that the absence of unliganded vitamin D receptor significantly impairs cWnt and hedgehog signaling pathways necessary for hair cycle initiation in VDR-null mice.

The vitamin D receptor helps control hair growth and may protect against certain skin tumors.

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.

In this study, distinct clinical responses and long-term resistances were observed in two pediatric patients with vitamin D-dependency type II, associated with abnormalities in their skin fibroblast interactions with 1,25-(OH)2D3.

In this case report, an ointment containing 1.24R-dihydroxyvitamin D3 was effective for treating follicular keratosis of the chin but did not provide lasting benefits after treatment ended.

This study presents the first reported Spanish case of Hypotrichosis with Juvenile Macular Dystrophy, identifying a new CDH3 mutation and highlighting the importance of clinical and genetic evaluation for accurate diagnosis.

This study found that while calcium can substitute for the Vitamin D receptor in maintaining epidermal keratinocyte differentiation, it cannot compensate for hair follicle dysfunction caused by the absence of the receptor.

This study identified a novel CDH3 mutation associated with sparse hair and pigmentary macular changes in two siblings with hypotrichosis but no visual symptoms.

In this study, a 68-year-old man with muscle-invasive bladder cancer and renal insufficiency achieved a partial radiological response to neoadjuvant therapy with gemcitabine and Disitamab Vedotin, without significant adverse events, highlighting a potential alternative for cisplatin-ineligible patients.

A genetic mutation caused severe rickets and alopecia in an Indian patient, but high-dose calcium and phosphate treatment improved their condition.

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 study found that deleting the vitamin D receptor from specific stem cells in mouse hair follicles disrupts their ability to regenerate the epidermis after injury, suggesting an essential interaction with the transcription factor p63.

This report describes a unique case of hereditary vitamin D-resistant rickets (HVDRR) in a dog, caused by a VDR gene mutation resulting in severe hypocalcemia and bone issues, which presented with symptoms similar to those observed in humans.

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.

This study found that after topical application in rats, 1,24-dihydroxyvitamin D3 absorbed through both the stratum corneum and hair follicles, with about 30% excreted via the faeces.

This study found that restoring vitamin D receptor expression in keratinocytes of VDR null mice prevents alopecia by enhancing the hair follicle's proliferative response during anagen initiation.

Vitamin D3 applied to mouse skin caused more wrinkles and sagging due to changes in the skin's outer layer.

A specific gene variant is linked to heart disease, increased heart muscle, curly hair, and thick skin on palms and soles.

This study found that the novel drug VDC-1101 showed a 45% objective response rate in treating canine cutaneous T-cell lymphoma, offering a potential treatment option for this challenging disease.

This description of dystrophy hypotrichosis associated with juvenile macular dystrophy provides an overview of this rare disorder characterized by short hair from birth and progressive loss of central vision but reports no new 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.