| [ Summary ] |
Pathogenesis of NASH profoundly involves oxidative stress caused by excess generation of reactive oxygen species (ROS) in the liver. In hepatocytes, ROS are generated by electron leakage during transportation, and the microsomal/peroxisomal β‒oxidation process. Innate immune cells in the hepatic microenvironment, such as Kupffer cells and infiltrating leukocytes, also produce a considerable amount of ROS in response to pathogen/damage associated molecular patterns (PAMPs/DAMPs). ROS not only facilitate fibrogenesis, but also trigger carcinogenesis in the liver. Thus, anti‒oxidant therapies, including administration of vitamin E, appears to be effective on prevention/treatment of NASH. |