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This study found that the vitamin D receptor, but not its ligand, regulates genes involved in hair cycle progression, suggesting a role in integrating hormone signaling pathways for hair and epidermal functions.

In this study, researchers found that syntaxin 9, a novel syntaxin family member, interacts specifically with the epidermal growth factor receptor and may influence its transport and signaling in some epithelial cells.

This study found that Celsr1, not Celsr2, is the primary protein involved in establishing planar cell polarity and hair follicle polarization in the epidermis of mice.

In this study, re-activating SOX9 in adult epidermal stem cells led to a fate switch towards hair follicle stem cell identity, with altered chromatin dynamics and oncogenic activation, contributing insights into developmental processes and cancer pathways.

This study found that EGCG improved the integrity of skin grafts during cryopreservation, suggesting its potential usefulness for skin preservation, though the exact mechanism remains unclear.

This study successfully developed 3D hair follicle organoids from neonatal mouse epidermal and dermal cells, showing structural and molecular resemblance to native anagen hair follicles.

In this study, the introduction of autofibroblasts into ischemic wounds was found to be slightly less favorable for regenerative histogenesis compared to a dermal equivalent with heterofibroblasts, with minor differences in epidermis thickness, collagen fiber area, and blood vessel area.

This study found that adding epidermal growth factor to mesenchymal stem cells enhanced wound healing and hair follicle regeneration in rats compared to stem cells alone.

This review discusses melanocyte stem cells in hair follicles and their potential role in cell-based therapy for vitiligo, reporting no new experimental results.

This study found that the medication dyclonine has a potent inhibitory effect on the TRPV3 channel, effectively rescuing cell death and alleviating pruritus symptoms in a mouse model with gain-of-function TRPV3 mutations, suggesting potential for treating skin inflammation.

This study observed that areola formation in mice requires exposure to pregnancy hormones and mechanical strain, beyond individual stimuli like hormonal milieu or strain alone.

This review examines emerging biomaterial strategies designed to support both neural regeneration and cutaneous wound healing, emphasizing their potential to improve sensory function through mechanisms like axonal regrowth and vascular network formation, while noting the need for standardized assessments and clinically translatable designs.

This study observed that, in mouse ear epidermal stem cells, a cell-autonomous size control mechanism involving the RB pathway dictates S phase entry timing based on cell size, despite external environmental variations affecting growth rates.

This study found that Krox20 marks a diverse stem cell population in mouse hair follicles, which significantly contributes to the interfollicular epidermis and regulates epidermal homeostasis.

This study found that deleting the Mof gene in mouse skin leads to severe defects in skin cell self-renewal, differentiation, and hair follicle growth, indicating that MOF is crucial for mitochondrial and ciliary gene expression and essential for skin development.

This review discusses the advancements needed for gene therapy to become commonly used in dermatology and reports no new clinical results.

This study found that Plakophilin 1 regulates innate immune responses in keratinocytes by controlling RNA helicase activity, balancing inflammation during epidermal immune challenges.

This review highlights emerging evidence that biophysical and metabolic cues, such as oxygen levels and tissue mechanics, significantly influence skin stem cell behavior, which is crucial for developing advanced wound healing therapies beyond traditional infection and inflammation control.

In this study, researchers used 3D bioprinting with skin stem cells and specific hydrogels to create artificial skin that successfully promoted complete wound healing and the regeneration of skin structures, including hair follicles and blood vessels, in mice.

In this study, researchers found that the expression of SLC1A6, a gene linked to calcium gradient and keratinocyte differentiation in the skin, significantly decreases with age, which may contribute to reduced skin barrier function in elderly individuals.

This study demonstrated that gene-corrected 3D skin constructs from RDEB patient-derived iPSCs, grafted onto immunocompetent mice, showed normal collagen VII expression after two months.

This study found that donor age and culture medium significantly impact the quality of human full-thickness skin models, with implications for their use as animal model alternatives in research.

This study found that STAT5 activation and Sox18 are key in regulating hair follicle induction and cycling, while transducing SKPs with active STAT5B improved wound healing by reducing inflammation.

SPRY1 deficiency in skin cells causes stem cells to move to the skin surface, leading to increased pigmentation.

This study found that abolishing H3K27me3 in mouse skin by targeting Ezh2 and Ezh1 affects hair follicle development and epidermal behavior, revealing functional differences between these tissues.

This study found that transient activation of c-Myc in transgenic mice stimulates keratinocyte proliferation and sebocyte differentiation, affecting normal epidermal and hair follicle development.

This study demonstrates that Sox2-positive dermal papilla cells specify particular hair follicle types by showing heterogeneity in gene expression and pathway activation in these cells.

This study found that Lgr5 and Lgr6 stem cells both activated wound-healing genes, but only Lgr5 stem cells changed their identity to contribute to new skin formation during wound repair.

This study describes a system for generating hair follicles from dissociated cells in mice, suggesting that successful development requires a foundational epithelial platform.

This study found that transgenic expression of COX-2 in mouse basal keratinocytes causes epidermal hyperplasia and certain dysplastic features at specific body sites.