ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
Macrophage β-catenin-Ihh axis induces hepatic stellate cell activation and fibrosis in metabolic dysfunction-associated steatohepatitis.
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
BACKGROUND &
aimsCurrently, there are no approaches to specifically target macrophage-hepatic stellate cell (HSC) crosstalk in metabolic dysfunction-associated steatohepatitis (MASH). Although the β-catenin signaling pathway has been implicated in fibrotic diseases, the role and downstream mechanism of macrophage β-catenin in MASH-associated hepatic fibrosis remains incompletely understood.
methodsMyeloid-specific β-catenin deficiency (β-catenin
resultsAlthough increased β-catenin activation was observed in the fibrotic liver macrophages of mice after HFD feeding, myeloid-specific β-catenin deficiency protected the liver against HFD-induced steatosis and fibrosis. Furthermore, we found that myeloid-specific β-catenin deficiency suppressed Ihh expression in liver macrophages. In vivo jetPEI-Man-mediated Ihh restoration prevented the improvement in MASH-induced fibrosis that we observed in β-catenin
conclusionOur findings identify the macrophage β-catenin-Ihh axis as a key regulator for controlling hepatic steatosis and fibrosis during MASH.
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