Under oxidative stress environment, mitochondrial function was impaired and excessive ROS production occurred, which further incurred damage to the mitochondria, leading to stress-induced apoptosis. Moreover, mitochondrial dysfunction leads to a decrease in NAD⁺ levels, which inhibits mitochondrial energy synthesis and Sirt3-mediated deacetylation of related proteins. Overexpression of NMNAT3 increases NAD⁺ remedial synthesis, promotes Sirt3-mediated deacetylation of mitochondria-related proteins, and increases mitochondrial energy synthesis and activation of antioxidant enzymes. Finally, it can improve the function of mitochondria and eliminate excessive ROS production, thereby inhibiting cellular stress-induced apoptosis.