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This study found that a specific VDR amino acid substitution in children with hereditary vitamin D-resistant rickets disrupts ligand binding and gene activation but does not impair hair follicle development.

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 found that VR1 activation in human hair follicles inhibited hair growth by suppressing proliferation and promoting apoptosis, suggesting VR1 plays an important role in hair growth regulation.

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.

In this study, homozygous VDR null mutant mice exhibited nonfunctional vitamin D receptors, leading to growth abnormalities and revealing the limited physiological importance of vitamin D pathways outside the classical receptor.

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 study found that neurotrophin-4 regulates Cav3.2 T-current expression in D-hair neurons via TrkB receptor activation, highlighting its role in mechanosensitive function.

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.

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 review article addresses how the TRPV4 ion channel helps cells respond to mechanical and environmental stimuli, discussing its role in calcium signaling crucial for tissue repair and fibrosis across various organ systems, and highlighting potential therapeutic targets from animal and disease models.

In this study, a novel VDR gene mutation was identified in a child with HVDRR, and the researchers observed that high-dose intravenous calcium therapy led to significant and sustained improvement in rickets symptoms.

This study found that the opioid system, particularly via the delta opioid receptor, broadly regulates cutaneous mechanosensation, including touch, and suggests targeting this receptor could alleviate injury-induced mechanical hypersensitivity.

This study suggests that in mice, plasmalogens may enhance hair growth by activating TRPC4 channels, which increases calcium influx and subsequently stimulates AMPK in hair follicles.

This study identified new genes and compounds affecting hair cell survival during ototoxin exposure using the zebrafish model, potentially aiding in understanding and preventing hearing loss and balance disorders in humans.

This study found that endothelin produced by hair follicle progenitors activates contractions in dermal sheath cells, facilitating hair follicle regression in the growth cycle.

NFATc1 is crucial for keeping hair follicle stem cells inactive.

This study found that low concentrations of CBD promoted hair follicle growth, while higher concentrations induced hair follicle regression and increased cell death in an experimental setting.

The researchers reported that both estrogen receptors ERα and ERβ are expressed in human testis, and identified two novel genes, Aven and Regucalcin, linked to estrogen and androgen regulation, which may be crucial for spermatogenesis.

Elevated luteinizing hormone contributes to female-pattern hair loss, and blocking certain channels may help prevent it.

This study found that elevated luteinizing hormone levels were significantly associated with female pattern hair loss, and implicated LH/LHR signaling in the aging and damage of hair follicles.

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.

This study observed that children with a genetically transmitted defect in the 1,25-dihydroxyvitamin D3 receptor experienced spontaneous healing of rickets as they aged, despite persistent mineral imbalances during treatment.

This study found that the vitamin D-VDR system is crucial for mineral and bone metabolism post-weaning and identified missense mutations in 1alpha-hydroxylase causing type I rickets.

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 this study, researchers used proteomic and metabolomic analyses to explore hair follicle development in embryonic cashmere goats, identifying significant roles for the oxytocin signalling pathway and associated networks in this process.

This study demonstrates that extracellular ATP induced by UV radiation promotes melanin production in human melanocytes, suggesting ATP-induced purinergic signaling may influence skin pigmentation.

This study reports that the epidermis is both a source and target for vitamin D3's active form, influencing skin and hair follicle differentiation through a calcium-mediated pathway.

This study reports that in mice, CaR plays a critical role in sensing the epidermal Ca2+ gradient, influencing keratinocyte differentiation, and affecting epidermal development.

This article reviews the role of vitamin D and its metabolites in regulating calcium homeostasis and highlights their effects on the intestine, kidney, bone, and parathyroid gland, without reporting new clinical results.

This review discusses the role of vitamin D and its receptor in maintaining skin and hair follicle health, but it reports no new clinical findings.