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Med."],"abstract":"<jats:p>Myocardial ischemia\u2013reperfusion injury (MIRI) is a critical pathological paradox following revascularization in acute myocardial infarction, yet effective clinical interventions remain limited. MIRI involves a complex, interlinked hierarchy of programmed cell death modalities, including ferroptosis, pyroptosis, and cuproptosis, which form a network mediated by the stimulator of interferon genes\u2013glutathione peroxidase 4 (STING\u2013GPX4), NOD-like receptor pyrin domain containing 3\u2013gasdermin D (NLRP3\u2013GSDMD), and sirtuin 3\u2013ATPase copper transporting alpha (SIRT3\u2013ATP7A) axes. The dynamic evolution of the immune microenvironment, mitochondrial dysfunction, and non-coding RNA regulatory networks further compound this. Emerging strategies, including bionanotechnology-enabled targeted delivery, intelligent responsive biomaterials, drug repurposing, genome editing, and precise ion channel modulation, demonstrate significant therapeutic potential. 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