Identification of effective cardiac biomarkers and therapeutic targets for myocardial infarction (MI) will play an important role in early diagnosis and improving prognosis. Ferroptosis, a cell death process driven by cellular metabolism and iron-dependent lipid peroxidation, has been implicated in diseases such as ischaemic organ damage, cancer and neurological diseases. Its modulators were involved in transferrin receptor, iron chelator, clock protein ARNTL, etc. Its mechanisms included the inhibition of system X_C⁻, diminished GPX4 activity, change of mitochondrial voltage-dependent anion channels and rising intracellular reactive oxygen species level. Further, the inhibitors of apoptosis, pyroptosis and autophagy did not prevent the occurrence of ferroptosis, but iron chelating agents and antioxidants could inhibit it. Noticeably, ferroptosis is an important pattern of cardiomyocyte death in the infarcted area, which may play a vital role in support of the myocardial pathological process of heart disease. However, the molecular mechanism of ferroptosis in the pathogenesis and the development of MI is not clear. Therefore, a greater depth of exploration of the mechanism of ferroptosis and its inhibitors will undoubtedly improve the pathological process of MI, which may be expected to identify ferroptosis as novel diagnostic and therapeutic targets of MI.

识别心肌梗死（MI）的有效心脏生物标志物和治疗靶点将在早期诊断和改善预后中发挥重要作用。铁死亡是一种由细胞代谢和铁依赖性脂质过氧化驱动的细胞死亡过程，与缺血性器官损伤、癌症和神经系统疾病等疾病有关。其调节剂参与转铁蛋白受体、铁螯合剂、时钟蛋白 ARNTL 等。其机制包括抑制系统 X _C ^-，GPX4活性降低，线粒体电压依赖性阴离子通道改变和细胞内活性氧水平升高。此外，细胞凋亡、细胞焦亡和自噬的抑制剂并不能阻止铁死亡的发生，但铁螯合剂和抗氧化剂可以抑制它。值得注意的是，铁死亡是梗死区心肌细胞死亡的一种重要模式，可能在支持心脏病的心肌病理过程中发挥重要作用。然而，铁死亡在心肌梗死发病和发展中的分子机制尚不清楚。因此，更深入地探索铁死亡及其抑制剂的机制无疑将改善心肌梗死的病理过程，有望将铁死亡确定为心肌梗死的新诊断和治疗靶点。