The activation of the mitochondrial ROS-NLRP3 inflammasome pathway in chronic kidney disease is a pivotal factor contributing to the apoptosis of renal tubular epithelial cells, while NRF2 exerts an antioxidant and anti-inflammatory role by attenuating mitochondrial ROS-mediated NLRP3 inflammasome activation, thereby mitigating high-fat-induced kidney injury [41]. This evidence concerns the gene NLRP3 and kidney injury.