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This study found that VEGF significantly promoted hair follicle growth and regeneration in mice with scleroderma.

This study reports that a prototype device may accurately measure changes in hair quantity, diameter, and density in patients with balding by assessing the cross-sectional area of hair bundles.

In this study, recombinant goat VEGF164 increased hair growth when applied to the skin of shaved mice.

This study reports that high-purity rHFSCs with strong proliferation and high VEGF165 expression can be efficiently obtained, facilitating tissue engineering applications like artificial hair follicles and skin construction.

This study found that rat hair follicle stem cells can be effectively transfected with VEGF 165 using lentivirus vectors, suggesting their potential use in developing tissue-engineered skin with improved vascularization.

In this study, VEGF165 induced hair follicle stem cells to differentiate into vascular endothelial cells, potentially supporting angiogenesis and neovascularization, with the Notch signaling pathway affecting differentiation efficiency.

This study found that transgenic mice expressing cgVEGF164 had increased hair follicle diameter and density, potentially linked to higher phosphorylation levels of ERK1/2, AKT1, and LEF1 proteins.

This study observed that VEGF165 increases proliferation and migration but alters adhesion properties of cultured human hair follicle cells, indicating a potential role for VEGF/VEGFR-2 in hair follicle regulation beyond angiogenesis.

Hair follicles in people with alopecia have lower levels of a key blood vessel growth protein.

In this study, transfection of the VEGF165 gene increased hair growth and rejuvenated the atrophic dermis in a mouse model of sclerotic skin.

This study reported a case of hereditary vitamin D–resistant rickets caused by a single heterozygous missense mutation in the VDR gene, showing dominant-negative effects and reduced response to 1,25-dihydroxyvitamin D3.

This study found that engineered extracellular vesicles (293F-EGF-EV), enriched in EGF mRNA, significantly aided skin wound healing in vitro and in a rat model by promoting fibroblast activity and improving wound recovery through processes like angiogenesis and reduced scarring.

This study found that VEGF stimulates the proliferation of human hair follicle dermal papilla cells via the VEGFR-2/ERK pathway, without involving p38, JNK, or AKT signaling.

This study found that VEGF, produced by human dermal papilla cells, can promote hair growth in vitro without increasing the proliferation of dermal papilla cells.

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.

This study found that a modified scaffold with VEGF165 genetically modified hair follicle stem cells significantly promoted blood vessel growth and wound healing in rats, suggesting its potential as a skin substitute in clinical settings.

This study found that human outer root sheath cells express VEGF receptor-2, and exogenous VEGF165 significantly stimulates their proliferation through activation of the ERK signaling pathway.

This study identified a novel I268T mutation in the vitamin D receptor that reduces its function, contributing to hereditary vitamin D-resistant rickets, and found that a potent vitamin D analog could improve receptor function.

This study found that the rs 1570360 polymorphism and the T-G-C haplotype of the VEGF gene may be associated with a protective factor against polycystic ovary syndrome in a Brazilian population.

This study describes a patient with hereditary vitamin D resistant rickets (HVDRR) who, despite having a truncated vitamin D receptor, did not exhibit typical hair or skin abnormalities, suggesting possible compensation via interactions with other proteins.

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 article discusses the development and clinical progress of PROTAC technology, particularly focusing on the New Drug Application for vepdegestrant, an estrogen receptor-targeting PROTAC, marking significant advancements in targeted protein degradation therapies.

This study created a humanized mouse model of hereditary vitamin D-resistant rickets that lacks alopecia, indicating the mutant receptor's potential to explore the syndrome's characteristics beyond vitamin D binding.

This study found that a novel R343H mutation in the vitamin D receptor gene impairs its transcription activity, contributing to hereditary vitamin D-resistant rickets and alopecia in the affected family.

This abstract reviews hereditary vitamin D-resistant rickets, a rare genetic condition causing severe early childhood rickets, and reports no new results; effective treatment typically requires high doses of calcium to address hypocalcemia and secondary hyperparathyroidism.

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.

In this case study, a girl with hereditary vitamin D resistant rickets had a novel mutation in the VDR gene that affected hair cycling without causing total alopecia, suggesting ligand-independent VDR function in hair cycling.

This study found that specific genes related to vascular endothelial growth factors are critical for feather maturity in certain chicken breeds, identifying key genetic markers that could enhance breeding efficiency.

This study found that using 3D Gel-C6S-HA scaffolds seeded with VEGF165-modified rat hair follicle stem cells enhanced angiogenesis and vascularization in tissue-engineered skin, improving wound healing.