FIG. 5.

NOX expression and function in liver fibrosis. The expression/activity of NOXs supports the increase in oxidative stress and altered redox signaling in the pathogenesis of liver fibrosis. NOX-generated ROS contribute to apoptosis and/or necrosis of hepatocytes after injury. Hepatocyte NOX-dependent ROS may activate hepatic Kupffer cells, resident macrophages of the liver. H₂O₂ and O₂· ⁻ from activated NOXs mediate the activation and transdifferentiation of HSCs into myofibroblasts, as well as in the phagocytosis of apoptotic bodies by HSCs. HSCs, hepatic stellate cells. Color images are available online.