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By inhibiting lipid ROS generation and the hyperpolarization of mitochondrial membrane potential, mitoglitazone could restore mitochondrial DNA copy number, the generation of ATP, and mitochondrial morphology in kidney tissue, inhibiting mitochondrial dysfunction and ferroptosis induced by I/R

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Future studies should integrate single-cell omics and organoid models to decode patient-specific mitochondrial dysfunction subtypes, enabling precise design of personalized therapies to bridge the gap from bench to bedside