Figure 4.

Triadic lesion in the pathogenesis of NASH. Hepatocyte injury, macrophage‐mediated inflammation, and hepatic stellate cell activation comprise the key mechanistic abnormalities in NASH. Soluble and EV signals from hepatocytes lead to proinflammatory activation of macrophages, can recruit proinflammatory monocytes into the liver, and also lead to hepatic stellate cell activation (depicted in red arrows). Other immune cells, such as neutrophils and B cells, may also respond to hepatocyte‐derived signals. Activated macrophages release cytokines and chemokines that can promote hepatocyte apoptosis, attract other immune cells into the liver, and also influence the activation of hepatic stellate cells. Abbreviation: ROS, reactive oxygen species.