In conclusion, in vitro and in vivo experiments indicated the prominent nephroprotective effects of PD against ferroptosis in Cis-AKI models, occurred at least partly through inhibiting excessive intracellular free iron accumulation and ROS production, rescuing GSH consumption, and enhancing GPx4 activity, thereby decreasing lipid peroxidation and ferroptosis sensitivity and ultimately attenuating the pathological progression of AKI. The gene discussed is GPX4; the disease is acute kidney injury.