Inflammasome activation triggers pyroptosis contributing to myocardial ischemia/reperfusion injury, making inflammasome pathways promising therapeutic targets.
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Myocardial ischemia/reperfusion injury, a prevalent sequela arising from reperfusion management of ischemic heart diseases, is characterized by regulated cardiomyocyte death processes. Pyroptosis is the outcome following inflammasome activation and constitutes a pivotal component of the pathology. Inflammasomes are large complexes of proteins that react to a variety of infectious or injury signals to achieve host defense through the immune system, while also acting as important mediators of myocardial ischemia/reperfusion injury. Here, we review recent advances in inflammasome classification, structure, and biological function. We further outline the cell-specific activation and spatiotemporal dynamics of inflammasomes in the heart following myocardial ischemia/reperfusion injury, and discuss their roles in myocardium tissue damage. We also focus on molecular mechanisms underlying ischemia/reperfusion-induced inflammasome activation. Finally, we explore the therapeutic potential of targeting the inflammasome pathway, review pertinent preclinical and clinical evidence, and assess the prospects and challenges for clinical translation.
Zhu et al. (Sun,) reported a other. Inflammasome activation triggers pyroptosis contributing to myocardial ischemia/reperfusion injury, making inflammasome pathways promising therapeutic targets.