Myocardial ischemia-reperfusion injury (MIRI) is one of the reasons for the high mortality in patients with acute myocardial infarction after percutaneous coronary intervention, which is regulated by several cell death pathways including apoptosis, autophagy, and pyroptosis. Recently, it has been found that ferroptosis, a unique programmed cell death, appears to be a therapeutic target for MIRI. However, the mechanisms remain incompletely elucidated. This review summarizes the latest research progress on the role of ferroptosis in MIRI, including mitochondrial dysfunction, endoplasmic reticulum stress (ERS), oxidative stress, calcium overload, epigenetic modification, apoptosis, autophagy, etc. Moreover, the signaling pathways between ferroptosis and MIRI are elaborated, which will provide new insights for the prevention and treatment of MIRI.