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Myocardial ischemia-reperfusion injury (MIRI) emerges when the restoration of blood flow fails to recover myocardial function following transient ischemia, marking a significant pathological challenge that adversely affects
revascularization outcomes and patient mortality. This condition often occurs post-cardiac procedures, including
cardiopulmonary bypass, angioplasty, primary percutaneous coronary intervention, and thrombolytic therapy. Over
the last decade, researches have been pivotal in deciphering the pathophysiological underpinnings of MIRI, aiming to identify viable targets and therapeutics for mitigation. Among these, pyroptosis, a form of inflammatory, programmed cell death, has been recognized for its integral role in MIRI, interacting with various other mechanisms
such as oxidative stress, calcium dysregulation, autophagy, ferroptosis, and apoptosis. This review delves into the
mechanisms by which pyroptosis influences MIRI, discusses its impact on both cardiomyocytes and non-cardiomyocytes in MIRI, and highlights recent advancements in the development of inhibitors targeting key molecules
involved in pyroptosis such as Nod-like receptor protein 3 inhibitors, Caspase-1 inhibitors, and traditional Chinese
medicines.
Keywords: Myocardial ischemia-reperfusion injury, pyroptosis, Nod-like receptor protein 3
