Myocardial ischemia–reperfusion (I/R) injury most commonly occurs in coronary artery disease when prompt reperfusion is used to salvage the ischemic myocardium. Cardiomyocyte death is a significant component of myocardial I/R injury and its mechanism was previously thought to be limited to apoptosis and necrosis. With the discovery of novel types of cell death, ferroptosis, necroptosis, and pyroptosis have been shown to be involved in myocardial I/R. These new forms of regulated cell death cause cardiomyocyte loss and exacerbate I/R injury by affecting reactive oxygen species (ROS) generation, calcium stress, and inflammatory cascades, subsequently mediating adverse remodeling, cardiac dysfunction, and heart failure. Herein, we review the roles of ferroptosis, necroptosis, and pyroptosis in myocardial I/R and discuss their contribution to pathology.

中文翻译：

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心肌缺血再灌注损伤中细胞死亡的调节

当立即再灌注用于挽救缺血心肌时，心肌缺血再灌注（I/R）损伤最常发生在冠状动脉疾病中。心肌细胞死亡是心肌I/R损伤的重要组成部分，此前认为其机制仅限于细胞凋亡和坏死。随着新型细胞死亡的发现，铁死亡、坏死性凋亡和细胞焦亡已被证明与心肌I/R有关。这些新形式的受调节细胞死亡通过影响活性氧（ROS）的产生、钙应激和炎症级联反应，导致心肌细胞损失并加剧缺血再灌注损伤，随后介导不良重塑、心功能障碍和心力衰竭。在此，我们回顾了铁死亡、坏死性凋亡和焦亡在心肌 I/R 中的作用，并讨论了它们对病理学的贡献。