Inflammasome activation and signalling in the ischemic-reperfused myocardium

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.