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The AMP\u2010activated protein kinase (AMPK) signalling pathway is considered a putative salvaging phenomenon, plays a decisive role in almost all cellular, metabolic, and survival functions, and therefore entails precise regulation of its activity. AMPK regulates various programmed cell death depending on the stimuli and context, including autophagy, apoptosis, necroptosis, and ferroptosis. There is substantial evidence suggesting that AMPK is down\u2010regulated in cardiac tissues of animals and humans with type 2 diabetes or metabolic syndrome compared to non\u2010diabetic control and that stimulation of AMPK (physiological or pharmacological) can ameliorate diabetes\u2010associated cardiovascular complications, such as myocardial ischemia\u2010reperfusion injury. Furthermore, AMPK is an exciting therapeutic target for developing novel drug candidates to treat cell death in diabetes\u2010associated myocardial ischemia\u2010reperfusion injury. Therefore, in this review, we summarized how AMPK regulates autophagic, apoptotic, necroptotic, and ferroptosis pathways in the context of myocardial ischemia\u2010reperfusion injury in the presence and absence of diabetes.<\/jats:p>","DOI":"10.1155\/2022\/7346699","type":"journal-article","created":{"date-parts":[[2022,10,11]],"date-time":"2022-10-11T19:06:20Z","timestamp":1665515180000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Role of AMPK in Myocardial Ischemia\u2010Reperfusion Injury\u2010Induced Cell Death in the Presence and Absence of 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