ArticleNature communications2026
Btg2 inhibits Fmo1 UFMylation thus exacerbating ferroptosis and apoptosis in hepatic ischemia-reperfusion injury.
Article in Nature communications, 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
Hepatic ischemia‒reperfusion injury (HIRI) represents a frequently occurring pathological condition during liver surgery, yet the mechanisms governing HIRI remain inadequately comprehended. Here, we investigate the role of B-cell translocation gene 2 (Btg2) in HIRI. Btg2 is upregulated following HIRI. A 70% HIRI model using hepatocyte-specific Btg2 transgenic and systemic Btg2 knockout mice reveals that Btg2 deteriorates hepatic inflammation and apoptosis. In primary hepatocytes, Btg2 knockdown reduces hypoxia/reoxygenation (H/R)-induced inflammation and mitochondrial stress. Metabolomics indicates that taurine metabolism is significantly affected in the livers of Btg2
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