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This study observed that piperonylic acid activated key signaling pathways in dermal papilla cells and increased hair growth markers, and a clinical trial showed users of a piperonylic acid formulation had more hair than those using a placebo, suggesting its potential for treating hair loss.

This report suggests that TCDD may alter human epidermal stem cell populations by upregulating c-Myc, potentially leading to increased stem cell turnover during chloracne development.

Activating Nrf2 can improve wound healing by increasing hair follicle stem cells.

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 found that Tideglusib enhances wound healing in aged rats by activating the PI3K/Akt pathway, suggesting its potential for medical and cosmetic applications targeting age-related skin changes.

This study found that epidermal growth factor significantly enhances the proliferation of hair follicle-derived mesenchymal stem cells through the EGFR/ERK and AKT pathways, without involving the STAT3 pathway.

In this study, researchers found that disrupting desmoglein 3 signaling in a mouse model of pemphigus vulgaris activates normally quiescent hair follicle stem cells, compromising their multipotency but prompting a regenerative response that restores stem cell function and structures.

In this study using a mouse model of Pemphigus vulgaris, researchers found that loss of desmoglein 3 adhesion in hair follicle stem cells triggers a regenerative program restoring stem cell function, requiring Hedgehog pathway suppression.

The researchers reported that SOX4 expression is significantly upregulated in melanoma and its knockdown in cell lines resulted in reduced tumor progression, suggesting potential for targeted therapies.

This study reported that in mouse models, deletion of EGFR resulted in stem cell hyper-proliferation followed by apoptosis, leading to scarring alopecia, and implicated EGFR's role in maintaining hair follicle quiescence and immune privilege during inflammation.

This study reported that EGFR activation leads to suppression of Stathmin, which may promote synchronized entry into catagen in hair follicles, highlighting potential mechanisms involving EGFR in hair cycle transitions.

In this study, EREG promoted hair growth by activating specific receptors in cell and animal models, indicating it may be a potential treatment for hair loss.

This study found that genetic activation of Nrf2 in keratinocytes accelerates wound repair by enhancing cell proliferation and re-epithelialization, suggesting potential use for Nrf2-activating compounds in individuals with impaired healing.

In this study, the researchers found that constitutive activation of the EGFR in mice led to increased sebum production, enlarged sebaceous glands, and altered gene expression related to sebocyte proliferation and lipogenesis.

This study found that in mice, EGFR activation suppresses mitotic regulators like Rcc2 and Stathmin 1, facilitating the transition to catagen in hair follicles.

The researchers concluded that baicalin may promote hair growth and follicle proliferation by activating the AKT pathway, suggesting its potential as a treatment for alopecia.

In this study, researchers found that androgen receptor activation in dermal papilla cells mainly affected the focal adhesion pathway and downregulated caveolin-1 gene expression, which could help identify new therapeutic targets for testosterone-related diseases.

In this study, topical piperonylic acid was found to improve wound healing in mice by activating EGFR and modulating gene expression related to the healing process.

This study reports that eliminating both Trp53 and Rb genes in mouse epidermis accelerates aggressive squamous cell carcinoma development due to early activation of the epidermal growth factor receptor/Akt pathway.

This study found that exosomes from human umbilical cord stem cells, pretreated with lithium chloride, significantly enhance hair regeneration in mice by activating the Wnt signaling pathway through miR-146a-5p.

This study found that the simultaneous inactivation of pRb and p53 genes in mouse epidermis accelerated aggressive squamous cell carcinoma development via activation of the epidermal growth factor receptor/Akt pathway.

In this study, topical application of piperonylic acid was observed to accelerate wound healing in mice by enhancing EGFR activation, keratinocyte modulation, and collagen deposition, suggesting its potential as a treatment for skin injuries.

This study suggests that EREG, released from ORS cells, may promote hair growth by activating specific receptors and modulating ROS generation, offering a potential new treatment for hair loss.

This article explores potential mechanisms of acneiform skin eruptions linked to EGFR inhibition in cancer patients, focusing on EGFR's role in controlling IL-1-dependent inflammation at hair follicles, but reports no clinical results.

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.

EGFR-targeted cancer therapy can cause skin issues starting at hair follicles, leading to inflammation.

This study reported significant transcriptomic changes in keratinocyte and immune cell populations in a mouse model with EGFR-deficient epidermis, suggesting possible targets for mitigating adverse skin events in EGFR-targeted cancer therapy.

This study explores how EGFR signaling impacts skin inflammation and follicular integrity during hair eruption, aiming to identify druggable pathways to mitigate skin inflammation in cancer patients receiving EGFR inhibitors.

In this study, the authors found that targeting mTORC1 with rapamycin inhibited TPA-induced skin tumor promotion by affecting keratinocyte proliferation, including critical stem cell populations in the mouse epidermis.