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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 study found that activating CB1 receptor signaling in human hair follicles increased stem cell proliferation while reducing differentiated cell survival, suggesting CB1's role as a survival stimulus for epithelial stem cells.

This study identified a nonfunctional Itpr3 gene in BTBR mice, attributed to a 12-bp deletion, which likely causes their simultaneous hair loss and taste perception deficits.

This study found that the transcription factor Gata6 plays a crucial role in adult mouse hair follicle regeneration by promoting the renewal and preventing DNA damage of rapidly proliferating progenitor cells.

This study found that quiescent bulge stem cells, when prevented from contributing to hair follicle and epidermal regeneration, did not affect hair follicle growth or wound healing in the short term.

In this study, researchers found that CD4 is expressed on murine K5⁺ keratinocytes, and its expression is crucial for maintaining epidermal stem cell balance and wound repair capacity, particularly during aging.

This study found that follistatin and activin interactions are important for hair follicle development and cycling in mice, suggesting that they may regulate processes involving BMP-2 and its antagonist.

This summary reports that γδ T cells play a role in regulating hair follicle formation during wound healing in adult skin.

This workshop review from the Australian Hair and Wool Research Society discusses findings in cutaneous biology and endocrinology but presents no new research results.

This study found that KLF4 expression in mouse hair follicle stem cells is important for effective cutaneous wound healing, with its knockdown leading to reduced stem cell populations and delayed healing.

This review discusses prolactin production and regulation in human skin and hair follicles, highlighting its potential broader implications but reports no new empirical results.

In this study, researchers reported that the activation of EDA2R by p53 leads to p53-dependent cell death in cancer cells and is involved in chemotherapy-induced hair loss.

This study suggests that the protease HAT-L4 plays a significant role in maintaining epidermal barrier function to prevent body fluid loss, as its absence in mice led to increased fluid loss and higher mortality.

IL-10 may worsen alopecia areata instead of helping it.

In this animal study, researchers found that the simultaneous deletion of ERBB2 and ERBB3 in mice results in impaired skin differentiation, inflammation, and sebaceous gland alteration, leading to skin lesions, while highlighting potential side effects in cancer therapies targeting these receptors.

This study demonstrated that blocking the Sonic hedgehog signaling pathway in mice led to reversible inhibition of body coat hair morphogenesis, while whisker development was unaffected.

This study suggests that extrasynaptic δGABA-A receptors may have a protective role in modulating the severity of catamenial-like seizures by influencing neurosteroid and benzodiazepine responses in mice.

This study found that deleting Snai2 and Snai3 genes in mice disrupts immune cell development, resulting in severe autoimmunity and early death due to the loss of immune tolerance.

This study reports that the peptide GPIGS, found in Bacillus sp. M18 conditioned medium, may promote hair growth through the PI-3K/Akt pathway and accelerate hair regrowth in mice.

This study found that endothelial TLR2 is crucial for effective angiogenesis and timely wound healing, whereas TLR2 in hair follicle stem cells is not essential for skin regeneration.

This research concluded that Snail2's absence in myeloid progenitors promotes tumor progression in mice, and specific zinc fingers are crucial for Snail1 and Snail2's roles in establishing epithelial-to-mesenchymal transition.

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.

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 on Sdr16c5/Sdr16c6-null mice found that inactivating these genes significantly increased Meibomian gland secretions and altered lipid profiles but had a subtle impact on sebogenesis, suggesting the genes control a bifurcation point in meibogenesis pathways.

This study found that proper levels of retinoic acid, controlled by the enzyme Cyp26b1, are essential for normal hair follicle development and morphogenesis in mice.

This study found that in mice, competition for hair follicles guides the organization of follicle-innervating LTMR neurons during early development, with different neuronal subtypes showing varying adaptive responses to increased neuron populations.

This study identified a genetic locus associated with rhabdomyosarcoma susceptibility in mice and found that specific differentiation markers are linked to the regression of basal cell carcinoma.

This study found that prolonged inhibition of DGAT1 in mice and dogs led to atrophy of sebaceous glands, with mice also experiencing alopecia, suggesting potential skin-related risks for humans using DGAT1 inhibitors.

This study found that ING5 knockout mice are prone to developing lymphomas and severe dermatitis, suggesting ING5 plays a role in tumor suppression and stem cell maintenance in vivo.

This study found that mice with a homozygous knockout of the Ten1 gene, developed through CRISPR-Cas9-mediated exon 3 deletion, exhibited telomere shortening and symptoms consistent with accelerated aging, such as reduced lifespan, skin changes, aplastic anemia, and cerebellar hypoplasia.