The etiology of non-alcoholic steatohepatitis (NASH) has been complicated. An increasing body of literature has indicated that hepatic oxidative stress exerts a causal role in driving NASH. Neverthele
We investigated the biological function of INSIG1 in acute (CCl4) and chronic (NASH) liver damage. Male whole-body Insig1 wild-type (WT), Heterozygous (HET) and Knock-out (KO) mice were: 1) challenged
Background & AimsPeriodontitis increases the risk of nonalcoholic fatty liver disease (NAFLD); however, the underlying mechanisms are unclear. Here, we show that gut dysbiosis induced by oral administ
