Findings from one investigation (Zhou L. et al., 2022) highlight PD’s significant renoprotective impact against ferroptosis in Cis-induced AKI models, achieved through multiple mechanisms: limiting excessive cellular iron accumulation, decreasing ROS generation, preserving GSH levels, boosting GPX4 functionality, thus minimizing lipid oxidation and ferroptotic susceptibility, ultimately decelerating AKI progression. Here, GPX4 is linked to acute kidney injury.