ArticleTranslational gastroenterology and hepatology2024
REGγ deficiency ameliorates hepatic ischemia and reperfusion injury in a mitochondrial p66shc dependent manner in mice.
Article in Translational gastroenterology and hepatology, 2024. 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: Hepatic ischemia and reperfusion (I/R) injury is a common problem faced by patients undergoing clinical liver transplantation and hepatectomy, but the specific mechanism of liver I/R injury has not been fully elucidated. The protein degradation complex 11S proteasome is involved in apoptosis, proliferation and cell cycle regulation by regulating the 11S proteasome regulatory complex (REG)γ. The main objective of this study is to explore the role and specific mechanism of REGγ in liver I/R. Methods: By constructing a model of Results: The expression of REGγ was up-regulated during hepatic I/R. REGγ KO had significantly reduced liver tissue infarct size, liver transaminases, inflammatory cells infiltration, inflammatory cytokine and activation of nuclear factor kappa-B (NF-κB) signaling pathway and cell apoptosis. REGγ KO had significantly alleviated the mitochondrial damage, decreased the up-regulated level of cytochrome C, reactive oxygen species (ROS). REGγ KO had significantly reduced p66shc mitochondrial translocation in mice. Conclusions: The experimental results of this study indicated that REGγ has an important role in preventing liver I/R injury and may play a role through the mitochondrial p66shc signaling pathway.
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