Figure 1.

Oxidative stress caused by mitochondrial structures and mt-DNA mutations in MAFLD. Activation of the mitochondrial membrane permeability transition pore (MPTP) by factors such as mitochondrial mutant genes and the accumulation of fatty acids promotes the outflow of Ca²⁺ from the mitochondrial calcium pool and then stimulates the activity of inner membrane proteins to affect the ATP synthesis rate and form new transition pores. Mitochondrial gene mutation (mt-DNA) also stimulates the activation of MPTP and uncoupling proteins (UCPs). In addition, the reduction in the activity of inner membrane proteins leads to electron leakage in the ETC, which promotes the generation of mt-ROS and ultimately aggravates the degree of mitochondrial oxidative stress in MAFLD.