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This review discusses the potential role of vitamin D supplementation as a therapeutic option for alopecia areata due to its immune-regulating effects and reports no new clinical results.

This case study reports on a rare form of vitamin D resistant rickets in a 37-year-old male, highlighting the condition's clinical features and the necessity for a thorough understanding of calcium and vitamin D metabolism in the diagnosis and management of metabolic bone diseases.

This case study reported that growth hormone therapy dramatically improved rickets symptoms and growth in three children with vitamin-D dependent rickets type 2 who had not responded to standard treatments.

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 study found that Danthron induced apoptosis in a human malignant melanoma cell line through mitochondrial, endoplasmic reticulum, and death receptor pathways.

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 review discusses the genetic causes and pathogenesis of Olmsted syndrome, emphasizing the potential for a genotype-phenotype correlation due to TRPV3 mutations, and explores avenues for individualized treatment developments for this condition.

This study developed an Asian human sebocyte cell line from breast skin tissue that can be used for sebaceous gland biology investigations, showing that Y27632 may promote cell growth through EGFR-CRAF-MEK-ERK and AKT pathways.

This study suggests that frontal fibrosing alopecia is a highly inflammatory disease involving TH1 and JAK-STAT pathways, without reduced hair keratins, highlighting JAK-STAT signaling as a potential therapeutic target.

Melatonin affects specific gene patterns and biological processes in goat hair growth.

This case study reports that a 3 ½ year-old male with vitamin D-dependent type II rickets showed partial improvement in alopecia and rickets when treated with high doses of 1,25(OH)2 vitamin D3.

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 suggests that 1,25-dihydroxyvitamin D(3) and fibroblast growth factor 23 form a crucial axis in regulating phosphate balance, akin to its role in calcium regulation, and explores novel VDR interactions including with curcumin.

This study found that SK2 channels in sensory terminals of rat muscle spindles and hair follicles may play a crucial role in modulating mechanosensory transduction by influencing receptor potentials through Ca2+-activated K+ currents.

This study found that Plant Elicitor Peptides enhance root hair growth through a mechanism independent of their known receptors, with PROPEP2 playing a key role in this process by influencing gene expression related to root hair formation.

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.

In this study, researchers concluded that hereditary 1,25-dihydroxyvitamin D-resistant rickets, characterized by specific mutations in the vitamin D receptor gene, may resolve metabolic abnormalities with age, though associated alopecia remains.

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 study used cryo-electron microscopy to reveal the structural mechanisms by which TRPV6 and TRPV3 ion channels open, close, and are regulated, providing insights for potential future research.

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.

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.

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 highlights a rare case of vitamin D-dependent rickets type 2A caused by a heterozygous mutation in the vitamin D receptor gene, emphasizing the complexity of managing this condition with high-dose calcium and vitamin D therapy.

This study suggests that αMSH may play a regulatory role in human dermal papilla cells, potentially influencing immune and inflammatory responses in hair follicles, which could contribute to inflammatory alopecia.

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 identified a novel V26M mutation in the vitamin D receptor as the cause of hereditary vitamin D resistant rickets in a patient, characterized by severe rickets and an unusual pattern of alopecia.

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 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 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 TRPV3 ion channels on human epidermal keratinocytes suppress cell proliferation, induce cell death, and trigger a proinflammatory response, suggesting a role in cutaneous inflammatory processes.