These findings not only establish a novel molecular theoretical foundation for targeting ferroptosis in the prevention and treatment of myocardial ischemia-reperfusion injury but also provide critical experimental evidence to support the translational application of S1P and its analogs—particularly fingolimod—in clinical management of acute myocardial infarction, through revealing the dynamic regulatory mechanism governing STAT3 phosphorylation at Tyr705. This evidence concerns the gene STAT3 and myocardial infarction.