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This study found that STAT5 activation in the dermal papilla acts as a key switch to trigger anagen entry in postdevelopmental hair follicle cycling.

This research reported that STAT5 activation in the dermal papilla plays a crucial role in triggering anagen entry during post-developmental hair follicle cycling.

This study found that constitutive activation of Stat3 in transgenic mice led to impaired hair growth and structural disorganization due to aberrant regulation of hair follicle and cytoskeletal genes.

This study found that constitutively active Stat3 in transgenic mice led to reduced keratinocyte stem cell populations in hair follicles, altering stem/progenitor cell dynamics and homeostasis.

Stat3 helps skin heal but can also cause skin diseases if overactive.

This study found that HPV8-induced actinic keratoses may mechanistically involve Lrig1+ hair follicle keratinocyte stem cells, with the E6 gene promoting downstream STAT3 activity in a mouse model.

In this study, Stat3 activation in transgenic mice led to a decrease in stem cells in the hair follicle bulge, suggesting its crucial role in epidermal growth and stem cell maintenance.

This study found that KRT6A expression increases after epidermal barrier disruption, worsening skin inflammation in disease conditions, and suggests that targeting KRT6A could offer a new treatment approach for inflammatory skin diseases linked to epidermal dysfunction.

This study found that Stat3 influences the differentiation and migration of keratinocytes, potentially impacting epithelial carcinogenesis, by examining Stat3 activation or deletion effects in mouse models.

This study found that intravenous administration of a shark-derived receptor antibody, 3P17, promoted hair growth in mice by increasing hair matrix cell proliferation and activating leptin-STAT3 signaling, with transdermal leptin delivery enhancing this effect through improved skin penetration.

The study reports that Fgf18 and Tgf-β2 signaling pathways in hair follicle stem cells have opposing effects on the timing of hair cycle transitions, influencing the shift from telogen to anagen phases.

This study found that phosphorylated VEGFR-2 is present in human scalp epidermal appendages and suggests it plays a role in their daily regulation.

This study found that adult mouse dermis can be reprogrammed by epidermal cues to resemble neonatal dermis, with changes in fibroblast proliferation and extracellular matrix composition.

Baricitinib reduces inflammation and mitochondrial damage in skin cells.

This study suggests that structural changes in the TRPV3 channel are linked to severe skin conditions like Olmsted syndrome, with differences observed between heat-activated and resting states.

In this study, researchers found that disrupting EGFR signaling in mice led to increased inflammation and hair follicle damage but that inhibiting the JAK-STAT1 pathway could restore hair growth and skin function.

This study found that in mice, hyper-activated JAK-STAT1 signaling due to EGFR inhibitor treatment leads to scarring alopecia, but JAK1/2 inhibition can restore hair follicle immune privilege and promote new hair growth.

This study demonstrated that anagen can be induced in Stat3-disrupted mice, suggesting that both Stat3-dependent and independent pathways, possibly involving PKC, mediate hair cycle progression with required PI3K activation.

This study reports that a new ROS-responsive hydrogel platform delivering miR-665 effectively reduced inflammation and promoted hair follicle regeneration in AA, suggesting a promising treatment approach.

This study demonstrated higher STAT3 gene expression in scalp tissue affected by androgenetic alopecia, but found no significant link with hair loss severity.

This study found that Runx1 in hair follicle stem cells modulates lipid metabolism, impacting membrane organization and enhancing signal transduction for cell proliferation in both normal and cancer epithelial cells.

In this study, a novel homozygous mutation in the STAT5B gene was identified in a 17-year-old boy with growth hormone-refractory growth failure, severe eczema, and autoimmune disease, suggesting a similarity to known STAT5B deficiency phenotypes.

This study found that Enz_MoriL, a compound derived from Morus alba L., promotes hair follicle cell proliferation by affecting the Wnt/β-catenin pathway and can counteract an alopecia areata-like condition by suppressing the JAK-STAT signaling in human hair follicle dermal papilla cells.

This review discusses the composition, activation, and regulation of the JAK/STAT pathway and highlights its role and inhibitors in various diseases, but reports no new experimental results.

In this study, activation of Tgr5 was found to improve alopecia areata and bone microstructure in mice by down-regulating the JAK1-STAT3 signaling pathway.

Targeting immune pathways like JAK/STAT may help treat frontal fibrosing alopecia.

This study observed that simvastatin promoted hair regrowth in a mouse model of alopecia areata by reducing inflammatory markers and T cell proliferation, partly through disruption of isoprenoid metabolite production.

This article, a special issue on hair follicle biology and pathology, reports no new research findings.

In this single-cell transcriptomic study, researchers analyzed AA scalp samples and found distinct immune and nonimmune cell activation patterns, with elevated TH1/TH2 and JAK/STAT markers potentially contributing to hair follicle immune privilege disruption and disease severity.