To elucidate the molecular mechanisms by which GPX4 regulates mitochondrial function, we overexpressed GPX4 in cardiomyocytes and subjected them to hypoxia-reoxygenation (H/R) modeling. Co-immunoprecipitation (Co-IP) coupled with liquid chromatography-tandem mass spectrometry (LC-MS/MS) was employed to identify potential partners of GPX4.