Cyp2e1, a cytochrome P450 enzyme, is involved in the metabolism of alcohol and other xenobiotics. It contributes to the generation of reactive oxygen species, leading to oxidative stress, and is associated with various biological processes and disease conditions [1,2,3,4,5,6].

In the context of alcoholic liver disease (ALD), studies using gene knockout (KO) mouse models have revealed important roles of Cyp2e1. In ERRγ -inducible FGF23-related ALD, hepatic CYP2E1 induction in response to alcohol is FGF23 dependent, and FGF23-LKO mice display decreased hepatic CYP2E1 expression and improved ALD through reduced hepatocyte apoptosis and oxidative stress [2]. Also, ethanol-induced fatty liver and oxidant stress in wild-type mice were blunted in CYP2E1 KO mice but restored in CYP2E1 knockin mice, indicating that Cyp2e1 contributes to ethanol-induced oxidant stress and liver injury [3]. Additionally, Cyp2e1 knockout mice are resistant to alcohol-induced gut leakiness and liver inflammation, suggesting its role in alcohol-induced gut permeability changes associated with ALD [4].

In conclusion, Cyp2e1 plays a crucial role in alcohol-related oxidative stress, liver injury, and gut permeability changes, as demonstrated by KO mouse models. These findings in ALD and other related conditions enhance our understanding of the biological functions of Cyp2e1 and its implications in disease development, providing potential therapeutic targets for treating associated diseases.