NEDD4L knockdown reduced lipid accumulation in non-alcoholic fatty liver disease by promoting the activity of PI3K/AKT signaling pathway.

ABSTRACT:

Background

Non-alcoholic fatty liver disease (NAFLD) represents a prevalent liver disease that influences the physical health of patients. Nonetheless, the exact pathogenesis of NAFLD remains unclear.

Object

To clarify how the neural precursor cell expressed developmentally downregulated 4-like (NEDD4L) regulates the lipid accumulation in the pathogenesis of NAFLD.

Methods

NAFLD mouse models received a high-fat diet (60% fat). NAFLD primary hepatocyte models were established by treating hepatocytes with oleate (OA). NEDD4L knockdown mice were purchased and fed a diet containing 60% fat. NEDD4L was silenced in primary hepatocytes by transfection. Liver tissues were stained via hematoxylin and eosin (HE). Primary hepatocytes and liver tissues were stained via Oil Red O.

SUBMITTER: Zhou J 

PROVIDER: S-EPMC12781842 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature