AI Article Synopsis
- Myocardial ischemia-reperfusion (I/R) injury typically occurs in coronary artery disease when restoring blood flow to previously ischemic heart tissue leads to cell death.
- Novel forms of regulated cell death—including ferroptosis, necroptosis, and pyroptosis—are involved in this injury, in addition to the previously known mechanisms of apoptosis and necrosis.
- These new cell death pathways worsen myocardial I/R injury by influencing oxidative stress, calcium imbalance, and inflammation, ultimately contributing to heart dysfunction and failure.
Article Abstract
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.
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| http://dx.doi.org/10.1016/j.tem.2023.10.010 | DOI Listing |
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