Reactive Oxygen Species as Key Molecules in the Pathogenesis of Alcoholic Fatty Liver Disease and Nonalcoholic Fatty Liver Disease: Future Perspectives
Zhiqing Zhang, Hong Yang, Fei Han, Peng Guo
Abstract
Reactive oxygen species (ROS) are central to the progression of alcoholic fatty liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD). In ALD, ROS arise from alcohol metabolism (CYP2E1 and ADH/ALDH2), causing oxidative damage and fibrosis. In NAFLD, mitochondrial dysfunction, ER stress, and lipotoxicity drive ROS overproduction due to metabolic dysregulation. Both diseases share ROS-mediated pathways, including mitochondrial/ER dysfunction, inflammation, and impaired lipid metabolism, accelerating steatosis to cirrhosis and cancer. Antioxidants, ER modulators, and lifestyle changes show therapeutic potential but require further clinical validation. Future research should leverage multi-omics and targeted therapies to optimize ROS-focused interventions for ALD and NAFLD.