Deletion of GPR81 activates CREB/Smad7 pathway and alleviates liver fibrosis in mice.

ABSTRACT:

Background

Enhanced glycolysis is a crucial metabolic event that drives the development of liver fibrosis, but the molecular mechanisms have not been fully understood. Lactate is the endproduct of glycolysis, which has recently been identified as a bioactive metabolite binding to G-protein-coupled receptor 81 (GPR81). We then questioned whether GPR81 is implicated in the development of liver fibrosis.

Methods

The level of GPR81 was determined in mice with carbon tetrachloride (CCl₄)-induced liver fibrosis and in transforming growth factor beta 1 (TGF-β1)-activated hepatic stellate cells (HSCs) LX-2. To investigate the significance of GPR81 in liver fibrosis, wild-type (WT) and GPR81 knockout (KO) mice were exposed to CCl₄, and then the degree of liver f

SUBMITTER: Zhi Y 

PROVIDER: S-EPMC11234765 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature