Serum amyloid A1 exacerbates hepatic steatosis via TLR4-mediated NF-κB signaling pathway

Abstract

These results demonstrate that SAA1 triggers hepatic steatosis and intrahepatic inflammatory response by forming a SAA1/TLR4/NF-κB/SAA1 feedforward regulatory circuit, which, in turn, leads to NAFLD progression. SAA1 may act as a potential target for the disease intervention.