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. 2018 Apr 25;8(4):390–402. doi: 10.1016/j.jceh.2018.04.001

Figure 1.

Figure 1

Pathophysiology of NAFLD. Visualized here are the influences of environmental factors, genetic components, and the intestinal microbiome on the development of hepatic steatosis and the progression of NAFLD. (A) NAFLD is characterized as >5% triglyceride accumulation in hepatocytes. This can be isolated hepatic steatosis, or accompanied by minimal inflammation within the lobules. (B) Histology showing classic features of NASH such as steatosis, inflammation, and hepatocellular ballooning degeneration. (C) Trichrome stain revealing progression of NASH to cirrhosis. (D) Histology illustrating the progression of cirrhosis to HCC. 11HSD-1, 11β-Hydroxysteroid Dehydrogenase Type 1; CCL2, C-C Motif Chemokine Ligand 2; EGF, Epidermal Growth Factor; FA, Fatty Acid; IL-6, Interleukin 6; HCC, Hepatocellular Carcinoma; HDL, High Density Lipoprotein; HGF, Hepatocyte Growth Factor; LDL, Low Density Lipoprotein; PAI-1, Plasminogen Activator Inhibitor-1; PDGF, Platelet-Derived Growth Factor; RBP4, Retinol Binding Protein 4; ROS, Reactive Oxygen Species; SNP, Single Nucleotide Polymorphism; TG, Triglyceride; TGF-β, Transforming Growth Factor Beta; TNF-α, Tumor Necrosis Factor Alpha.