Fig. 2

Pathological mechanisms of NAFLD and main models in zebrafish. Possible pathological mechanisms of steatosis in NAFLD induced by diets, insulin resistance, pathogens and hepatoxic drugs, and the effects of mitochondrial dysfunction, endoplasmic reticulum stress and inflammatory cell infiltration which lead to inflammation, fibrosis and apoptosis in hepatocytes. The diet models, transgenic and mutation models involved are shown in the figure. ACC, acetyl-CoA carboxylase; CHOP, CCAAT/enhancer-binding protein homologous protein; CM, chylomicron; DAGs, diacylglycerols; DNL, de novo lipogenesis; EDCs, endocrine-disrupting chemicals; ER, endoplasmic reticulum; FFA, free fatty acid; FAS, fatty acid synthase; FXR, farnesoid X receptor; HBV, hepatitis B virus; HSC, hepatic stellate cell; JAK-STAT, Janus kinase/signal transducer and activator of transcription; JUNK, Jun amino-terminal kinase; LPCs, lysophosphatidylcholines; LXR, liver X receptors; MO, morpholino; mTOR, mechanistic target of rapamycin; PPAR, peroxisome proliferators-activated receptors; ROS, reactive oxygen species; SCD, stearoyl-CoA desaturase; SREBP-1C, sterol regulatory element binding protein 1c; TG, triglyceride; UPR, unfolded protein response; VLDL, very low-density lipoprotein.