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This study reported that UVR induced PKCε phosphorylation of Stat3 in transgenic mice, suggesting a role in enhancing sensitivity to UVR-related skin cancer development.

This study found that 3-Deoxysappanchalcone may stimulate hair growth in mice by promoting proliferation of hair follicle dermal papilla cells through WNT/β-catenin and STAT signaling modulation.

This study found that Hirosaki hairless rats experience transient activation of STAT5A in the mammary glands during early lactation, involving O-GlcNAc modification rather than Tyr-phosphorylation.

This study observed that Epigallocatechin-3-gallate (EGCG) can inhibit phosphorylation of STAT1 and reduce a specific subset of immune cells in vitro and ex vivo, suggesting a potential role in maintaining immune privilege in alopecia areata.

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 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.

The study reports that vitamin E improves hair-follicle growth and dermal papilla cell proliferation in vitro by modulating the lncRNA2919/STAT1/SHH axis in Angora rabbits, enhancing cellular antioxidant capacity.

In this study, researchers found that minoxidil sulfate enhances the anti-inflammatory effects of the JAK inhibitor baricitinib in alopecia areata, modulating inflammatory signals and preserving immune privilege features in human hair cells, which suggests potential benefits for combined therapy.

In this study, the researchers using Shh-GFP^+/- mice found that cyclophosphamide-induced alopecia involves the JAK/STAT1 pathway, where STAT1 binds the Shh gene promoter, decreasing Shh-expressing cells in hair follicles. Treatment with JAK inhibitors helped rescue hair loss, implicating the JAK/STAT1 pathway in this process.

This study demonstrated that disrupting EGFR signaling in mice leads to immune sensitivity compromising the hair follicle's protective environment, but JAK1/2 inhibition can restore this immune privilege and stimulate hair growth, suggesting a potential therapy for scarring hair loss diseases like cicatricial alopecia.

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 research found that kaempferol, a flavonoid from hair growth-promoting plants, significantly enhanced human dermal papilla cell proliferation and inhibited specific signaling pathways, outperforming minoxidil, with topical application in mice promoting hair growth and thickness, indicating potential as a natural hair loss treatment.

This study suggests that particulate matter can induce inflammation in human outer root sheath cells, potentially affecting hair growth, through oxidative stress-dependent MAPK and JAK-STAT signaling pathways.

This study found that elevated STAT5 levels are linked to improved hair-inducing capabilities in human dermal papilla cells, and reducing STAT5 impairs hair follicle induction.

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

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 found that disrupting Stat3 in keratinocyte stem cells of mice reduced skin tumor formation by approximately 80%, suggesting Stat3's role in tumor initiation survival mechanisms.

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 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.

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.

This study found that the hair interior defect in AKR/J mice is linked to a mutation in the Soat1 gene, which disrupts SOAT1 protein expression and affects lipid metabolism critical for normal hair formation.

This study suggests that NFIB and STAT5 work together to control cell-specific genetic programs in mammalian tissues, particularly in mammary and hair follicle stem cells.

This study found that IL-6 knockout mice exhibited increased wound-induced hair neogenesis compared to wild-type mice, likely due to enhanced STAT3 activation facilitated by compensatory cytokine activity.

This study found that a titrated extract of Centella asiatica enhanced the hair growth potential of 3D spheroid cultured human dermal papilla cells.

This study reported that IL-6/STAT3 signaling influences p63 isoform expression in keratinocytes and is involved in wound-induced hair follicle neogenesis, highlighting the interplay between immune and developmental pathways.

In this study, Gsdma1/2/3 knockout mice showed reduced epidermal hyperplasia and inflammation when induced by PMA, which was attributed to decreased EGFR-Stat3/Akt signaling due to a decrease in related ligands.

In this study, Lagerstroemia indica extract was found to significantly promote hair growth and prevent hair loss in human trials, likely through the regulation of specific signaling pathways, indicating its potential as a cosmetic treatment for hair loss prevention.

This study suggests that STAT3 signaling in keratinocytes is crucial for maintaining skin homeostasis by regulating hair follicle-specific keratin genes, potentially impacting dermatitis development through microbe-triggered inflammatory responses.

This study found that saw palmetto extract inhibits glioma cell proliferation and angiogenesis via the STAT3 pathway, suggesting its potential use as a complementary therapy for cancers with activated STAT3 signaling.

This study reports that Broussonetia papyrifera extract significantly increased hair count over 12 weeks in a small clinical trial and promoted dermal papilla cell proliferation in vitro by regulating WNT-β-catenin and STAT6 pathways.