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Review
. 2021 Oct 23:2021:9929687.
doi: 10.1155/2021/9929687. eCollection 2021.

Ferroptosis: Opportunities and Challenges in Myocardial Ischemia-Reperfusion Injury

Wei-Kun Zhao  1 , Yao Zhou  2   3 , Tong-Tong Xu  1 , Qi Wu  4
Affiliations
Review

Ferroptosis: Opportunities and Challenges in Myocardial Ischemia-Reperfusion Injury

Wei-Kun Zhao et al. Oxid Med Cell Longev. .

Abstract

Ferroptosis is a newly discovered form of regulated cell death dependent on iron and reactive oxygen species (ROS). It directly or indirectly affects the activity of glutathione peroxidases (GPXs) under the induction of small molecules, causing membrane lipid peroxidation due to redox imbalances and excessive ROS accumulation, damaging the integrity of cell membranes. Ferroptosis is mainly characterized by mitochondrial shrinkage, increased density of bilayer membranes, and the accumulation of lipid peroxidation. Myocardial ischemia-reperfusion injury (MIRI) is an unavoidable risk event for acute myocardial infarction. Ferroptosis is closely associated with MIRI, and this relationship is discussed in detail here. This review systematically summarizes the process of ferroptosis and the latest research progress on the role of ferroptosis in MIRI to provide new ideas for the prevention and treatment of MIRI.

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Conflict of interest statement

The authors declare that they have no conflicts of interest.

Figures

Figure 1
Figure 1
Cartoon depicting the possible mechanism and regulation of ferroptosis. Ferroptosis is mainly regulated by Fe homeostasis, lipid oxidation, System Xc−, and VDAC. The most important in the ferroptosis signaling pathway is the production of iron ions and ROS. GPX-4 is a key regulator of ferroptosis. Inhibition of GPX-4 causes a large amount of lipid peroxides to aggregate, becoming a sign of ferroptosis.
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