ArticleJournal of molecular medicine (Berlin, Germany)2026
Kv1.3 regulates macrophage immune function through PI3K/AKT signaling pathway to alleviate metabolic dysfunction-associated steatohepatitis.
Article in Journal of molecular medicine (Berlin, Germany), 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
BACKGROUND AND
aimThe progression of metabolic dysfunction-associated steatohepatitis (MASH) is closely linked to macrophage-mediated inflammatory responses. The role of Kv1.3, a key voltage-gated potassium channel regulating macrophage function, in MASH remains unclear. This study investigated Kv1.3 blockade's therapeutic potential in MASH and its mechanism, focusing on the PI3K/AKT signaling pathway.
methodsA Western diet (WD)-induced mouse model of MASH was established, and hepatic Kv1.3 was knocked down via AAV8-Kv1.3-shRNA. Hepatic steatosis, inflammation, and macrophage infiltration were evaluated. In vitro, LPS-stimulated RAW264.7 macrophages were treated with the Kv1.3 inhibitor ShK-186 to assess inflammatory cytokine (IL-6, TNF-α) production and migration. The GEO dataset (GSE222922) validated the PI3K/AKT signaling pathway involvement.
resultsKv1.3 expression was significantly increased in WD-induced MASH mouse livers. Hepatic Kv1.3 knockdown alleviated liver injury, steatosis, and inflammation. In vitro, ShK-186 inhibited LPS-induced macrophage migration and cytokine production, and significantly reduced the PI3K/AKT phosphorylation. These effects were reversed by the PI3K agonist 740Y-P, confirming that Kv1.3 regulates macrophage function via the PI3K/AKT signaling.
conclusionKv1.3 modulates macrophage inflammation and migration through the PI3K/AKT signaling pathway, promoting MASH progression. Kv1.3 knockdown ameliorates MASH pathology, highlighting it as a promising therapeutic target. KEY MESSAGES: Kv1.3 drives MASH via macrophage PI3K/AKT signaling, worsening liver inflammation Macrophage Kv1.3 knockdown alleviates MASH pathology in WD-fed mice Kv1.3 is a potential therapeutic target for MASH, modulating liver inflammation.
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