Schisandrin B: A Double-Edged Sword in Nonalcoholic Fatty Liver Disease

Figure 1

The pathogenesis of nonalcoholic fatty liver disease (NAFLD). The percentage shown along the arrow indicates the prevalence of the pathogenesis leading to the next stage of NAFLD. Hallmarks and important features of each stage of NAFLD are indicated. Insulin resistance is an important pathological factor for the development of hepatic steatosis (a benign stage of NAFLD), presumably due to the induction of hepatic de novo lipogenesis as well as lipolysis of adipose tissue. Key enzymes involved in these processes are indicated (in pink box). Changes in the profile of adipokines and cytokine, dysbiosis of gut microbiota, hepatic oxidative stress/inflammation, and endoplasmic reticulum ER stress are regarded as the “multiple parallel hits” of the pathogenesis of NASH from hepatic steatosis. Key factors involved in the pathogenesis are indicated (in orange box). SREBP1: sterol regulatory element-binding protein-1; ACC: acetyl-CoA carboxylase; FAS: fatty acid synthase; ATGL: adipose triglyceride lipase; HSL: hormone-sensitive lipase; GI tract: gastrointestinal tract; TNF-α: tumor necrosis factor-α; IL-6: interleukin-6; ROS: reactive oxygen species; ER: endoplasmic reticulum; PDGF: platelet-derived growth factor; TGF-β: transforming growth factor-β; ECM: extracellular matrix.