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
 
                
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