MyD88 orchestrates fatty acid metabolism in tumor-associated macrophages and non-alcoholic fatty liver disease-related hepatocarcinogenesis.

ABSTRACT:

Introduction

Non-alcoholic fatty liver disease (NAFLD) is a growing cause of cirrhosis and hepatocellular carcinoma (HCC). Toll-like receptors (TLRs) and their adapter protein, myeloid differentiation factor 88 (MyD88), are activated in NAFLD and contribute to its development. However, the specific role of MyD88 in myeloid cells that regulate NAFLD-associated hepatocarcinogenesis remains unknown.

Methods

We used a diethylnitrosamine/high-fat diet-induced HCC mouse model with selective deletion of MyD88 from myeloid cells to investigate NAFLD-HCC, and we evaluated the development of NAFLD-HCC histologically and genetically.

Results

Myeloid cell MyD88-deficient (Lyz^MyD88-/-) mice were protected from diet-induced obesity and developed fewer and smaller liver t

SUBMITTER: Chen H 

PROVIDER: S-EPMC12500666 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature