Activation of the STING-IRF3 pathway promotes hepatocyte inflammation, apoptosis and induces metabolic disorders in nonalcoholic fatty liver disease

Article ID	Journal	Published Year	Pages	File Type
8633061	Metabolism	2018	27 Pages	PDF

Abstract

Our results suggest that the STING-IRF3 pathway promotes hepatocyte injury and dysfunction by inducing inflammation and apoptosis and by disturbing glucose and lipid metabolism. This pathway may be a novel therapeutic target for preventing NAFLD development and progression.

Keywords

HFD PFK IPITT IRF3 NCD TRAF6 PEPCK p-GSK3β GCK NAFLD PPARα LDL-C ALT FFA SREBP-1c G-6-Pase DMEM NF-κB FBS PBS AUC IPGTT Dulbecco's modified Eagle's medium Small interfering RNA siRNA intraperitoneal insulin tolerance test intraperitoneal glucose tolerance test AST Aspartate aminotransferase Alanine aminotransferase Free fatty acid inflammation immunohistochemical IHC interferon IFN interleukin Nonalcoholic fatty liver disease triglyceride tumor necrosis factor alpha Apoptosis high-fat diet normal chow diet fetal bovine serum Interferon regulatory factor 3 TNF receptor-associated factor 6 TNF-α nuclear factor κB Phosphate buffered saline phospho-glycogen synthase kinase-3β phosphoenolpyruvate carboxykinase Phosphofructokinase Glucose and lipid metabolism stimulator of interferon genes area under the curve STING body weight Sterol regulatory element binding protein-1c pyruvate carboxylase pyruvate kinase total cholesterol Low-density lipoprotein-cholesterol negative control glucose-6-phosphatase Glucokinase peroxisome proliferator-activated receptor α