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• W2091283163 abstract "Abstract Background & Aims Acute liver failure ( ALF ) is a condition with high mortality and morbidity. Fibrosis in chronic liver disease was extensively researched, whereas fibrosis and underlying mechanism in acute liver failure remains unclear. Methods Hepatitis B virus related ALF patients were recruited to investigate if there was ongoing fibrosis by liver histology and liver stiffness measurement(LSM) analysis as well as fibrosis markers assay. Sera HMGB1 were kinetically detected in progression and remission stage of ALF. Hepatic stellate cell(HSC) activation by HMGB1 was explored by testing mRNA and protein level of α‐SMA and collagen 1a1 by using qPCR and western blot. Autophagy induction by HMGB1 was explored by LC3‐II conversion, autophagy flux and fluorescence. Results Firstly, ongoing fibrosis in progression stage of ALF was confirmed by histological analysis, LS measurement as well as fibrosis markers detection. HSC activation and autophagy induction in explanted liver tissue also revealed. Next, kinetic monitoring sera HMGB1 revealed elevated HMGB1 in progression stage of ALF vs HBsAg carrier, and drop back to base level in remission stage. Thirdly, rHMGB 1 dose dependently activated HSCs, as indicated by increased mRNA and proteins level in α‐SMA and collagen 1a1. Moreover, autophagy was induced in HSC treated with rHMGB 1, as illustrated by increased LC3 lipidation, elevated autophagy flux and GFP‐LC3 puncta. Conclusions Acute liver failure is accompanied by ongoing fibrosis, HSC activation and autophagy induction. Increased HMGB 1 activates HSC via autophagy induction. Those findings integrate HMGB 1, HSC s activation, autophagy into a common framework that underlies the fibrosis in ALF ." @default.
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• W2091283163 date "2015-01-22" @default.
• W2091283163 modified "2023-10-12" @default.
• W2091283163 title "Mechanisms of fibrosis in acute liver failure" @default.
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• W2091283163 doi "https://doi.org/10.1111/liv.12731" @default.
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