JMIR Publications

ABSTRACT

Identification of effective cardiac biomarkers and therapeutic targets for myocardial infarction (MI) will play an important role in early diagnosis and the 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, and clock protein ARNTL, etc. Its mechanisms included the inhibition of the system XC-, the diminished GPX4 activity, the change of mitochondrial voltage-dependent anion channels, and the rising intracellular ROS level, etc. 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 myocardial pathological process of heart disease. However, the molecular mechanism of ferroptosis in the pathogenesis and development of MI is not clear. Therefore, a greater depth of exploration of the mechanism of ferroptosis in MI and ferroptosis inhibitors will undoubtedly improve the pathological process of MI, which is expected to identify ferroptosis as novel diagnostic and therapeutic targets of MI.