Loss of long-chain acyl-CoA synthetase 1 promotes hepatocyte death in alcohol-induced steatohepatitis.

ABSTRACT:

Background

Alcohol consumption has been shown to disrupt hepatic lipid homeostasis. Long-chain acyl-CoA synthetase 1 (ACSL1) critically regulates hepatic fatty acid metabolism and lipid homeostasis by channeling fatty acids to lipid metabolic pathways. However, it remains unclear how ACSL1 contributes to the development of alcohol-associated liver disease (ALD).

Methods

We performed chronic alcohol feeding animal studies with hepatocyte-specific ACSL1 knockout (ACSL1^Δhep) mice, hepatocyte-specific STAT5 knockout (STAT5^Δhep) mice, and ACSL1^Δhep based-STAT5B overexpression (Stat5b-OE) mice. Cell studies were conducted to define the causal role of ACSL1 deficiency in the pathogenesis of alcohol-induced liver injury. The clinical relevance of the

SUBMITTER: Dong H 

PROVIDER: S-EPMC10245388 | biostudies-literature | 2023 Jan

REPOSITORIES: biostudies-literature