ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
Targeting the TOPK-STAT3 pathway in keratinocytes and mast cells mediates the therapeutic attenuation of Atopic dermatitis.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAtopic Dermatitis (AD) is a prevalent chronic inflammatory skin disorder with incompletely understood pathogenesis and limited therapeutic options. T-Lymphokine-Activated Killer Cell-Originated Protein Kinase (TOPK) is known to promote inflammation, its specific role in AD remains unclear. This study sought to elucidate the function of TOPK in AD pathogenesis and to delineate its underlying molecular mechanisms.
methodsTOPK expression in AD patients was analyzed using the Gene Expression Omnibus (GEO) database. The functional role of TOPK in AD pathogenesis was investigated through genetic knockdown and pharmacological inhibition in a relevant disease model. Mechanistic insights were obtained via phosphoproteomic profiling, interaction assays (co‑immunoprecipitation and pull‑down), and kinase assays. The cellular function of the TOPK‑driven pathway was further validated by inhibiting TOPK in both HaCaT keratinocytes and mast cells.
resultsBioinformatics analysis revealed that TOPK was significantly upregulated in AD patients. Genetic or pharmacological inhibition of TOPK markedly attenuated AD-like pathological features and reduces the levels of IgE, IL-6, IL-8 and IL-33, suggesting that TOPK contributes to AD pathogenesis. Mechanistically, TOPK was found to directly interact with and phosphorylate STAT3 at Ser727. Inhibition of TOPK in both HaCaT keratinocytes and mast cells decreased STAT3 phosphorylation at Ser727, thereby alleviating AD-related inflammatory responses. These findings validate the central role of the TOPK-STAT3 signaling pathway in regulating key inflammatory responses in AD.
conclusionIn summary, TOPK drives AD pathogenesis by phosphorylating STAT3 at Ser727, highlighting its promise as a therapeutic target. Genetic or pharmacological inhibition of TOPK suppresses this signaling axis, alleviates AD‑associated inflammation, and provides a promising new strategy for clinical intervention.
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