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In this review, we synthesize the current understanding of how dysregulated copper metabolism and cuproptosis drive the pathogenesis of major cardiovascular conditions, including myocardial ischemia/reperfusion (I/R) injury, anthracycline-induced cardiotoxicity, atherosclerosis, diabetic cardiomyopathy (DCM), and sepsis-induced cardiac dysfunction, through pathways such as mitochondrial dysfunction, oxidative stress, and inflammation