Abstract Body (Do not enter title and authors here): Acute myocardial infarction (AMI), a leading cause of morbidity and mortality, is often caused by occlusion of the left anterior descending (LAD) artery, resulting in ischemia and cardiomyocyte death. While apoptosis has been widely studied, recent evidence implicates ferroptosis as a critical contributor to myocardial injury, though its precise role in AMI remains unclear. This study investigated the cardioprotective effects of ferrostatin-1 (Fer-1), a ferroptosis inhibitor, in a rat model of AMI induced by LAD ligation. Rats were divided into four groups: control, Fer-1, AMI, AMI with Fer-1 (n = 7 per group). Following 15 minutes of LAD ligation, Fer-1 was administered, and the rats were reperfused for 15 minutes before being sacrificed. Myocardial damage was evaluated using TTC staining and by measuring serum creatine kinase (CK) and lactate dehydrogenase (LDH) levels. Our results showed that AMI significantly increased infarct size (by > 20%), along with CK and LDH levels (all p < 0.001) compared to controls. Additionally, mRNA expression of ferroptosis-related markers xCT and GPX4 was analyzed via real-time PCR. Both xCT and GPX4 mRNA expression were significantly downregulated in AMI (all p < 0.001). Furthermore, echocardiography revealed that AMI markedly reduced ejection fraction (EF) and fractional shortening (FS), indicating impaired left ventricular systolic function. Fer-1 treatment significantly improved EF and FS compared to the AMI group (all p < 0.05), demonstrating its functional cardioprotective effects. Statistical analyses were performed using the Mann-Whitney U test and one-way ANOVA with Bonferroni post-hoc correction (p < 0.05). These findings highlight the significant cardioprotective effects of Fer-1 against AMI and suggest its potential as a diagnostic biomarker and therapeutic target.