Furthermore, PINK1-deficiency or PARK2-deficiency promoted mitochondrial injury, mitochondrial ROS, RTEC apoptosis, and NLRP3 inflammasome activation induced by contrast exposure in an in vivo and in vitro CI-AKI mice model, indicating that PINK1–Parkin-mediated mitophagy could improve CI-AKI by inhibiting mitochondrial injury, mitochondrial ROS, RTEC apoptosis, NLRP3 inflammasome activation, and renal damage induced by contrast exposure. The gene discussed is PRKN; the disease is acute kidney injury.