Mechanisms in Exercise Intervening NAFLD:Mitohormesis of ROS-induced UPRmt

Non-alcoholic fatty liver disease(NAFLD) is a severe but underestimated health threat in the world, and there is no FDA approved effective pharmacologic agents currently. Therefore, it is urgent to study its pathogenesis and explore treatment strategies.Research shows that oxidative stress is implicated in the development of NAFLD, and the mitochondria ROS production and homeostasis are crucial for the prevention and treatment of NAFLD. Aerobic exercise or lipid deposition can change the ROS level in cells, and the regulation of different ROS levels on mitochondrial unfolded protein response(UPRmt) is defined as“mitohormesis”. The slight disturbance in mitochondrial homeostasis will promote the “crosstalk” between the coordinating mitochondria and the nucleus, and then reduce the sensitivity of cells to external stimuli and improve the ability of cells to resist stimuli. Future research should investigate the molecular mechanism of exercise induced UPRmt activation and mitokines secretion through ROS regulated elF2α-ATF4/5-CHOP pathway, and to illuminate the effect of exercise on ROS-UPRmt regulatory mechanism and mitochondrial homeostasis maintenance, thus providing theoretical references for the prevention and control of NAFLD.