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This review explores the shared pathogenesis of alopecia areata and vitiligo and compares treatment responses, noting that hair regrowth in alopecia areata occurs more rapidly than skin re-pigmentation in vitiligo, possibly due to differences in stem cell biology and treatment effects on melanocytes.

This review discusses how dental pulp stem cells and their derivatives may accelerate skin wound healing by modulating inflammation, promoting angiogenesis, optimizing extracellular matrix structure, and enhancing tissue formation, with implications for translating these findings into therapies for skin and mucosal repair.

This research discusses the shift in cosmetic dermatology towards integrating regenerative medicine, AI, and personalized care, highlighting their potential to improve aesthetic outcomes and skin function while considering ethical and regulatory challenges.

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 review discusses keratin disorders and potential RNA interference therapeutics, reporting no new clinical findings but highlighting the promise of siRNA for future treatments.

This review discusses the similarities and differences in wound healing between non-sterile skin wounds and ischemic injuries to internal organs, emphasizing regenerative capabilities observed in zebrafish models, with no new clinical results reported.

In this study, it was observed that NIPAL4 mutations linked to autosomal recessive congenital ichthyosis lead to abnormal skin barrier function due to cytotoxic effects disrupting lipid structure and organization, which topical treatments only partially ameliorated.

This study found that specific gene upregulations and mutations in hidradenitis suppurativa skin support the role of inflammation, altered epithelial differentiation, and metabolism dysregulation in the disease's pathogenesis.

In this study, around 1% of proteins in skin fibroblasts significantly changed in response to reductive stress, affecting collagens and MAPK signaling pathways.

This study found that exposure to 12-O-tetradecanoyl-phorbol-13-acetate in mouse skin caused changes in claudin expression and localization, indicating disruption and eventual recovery of the epidermal barrier.