Myocardial ischemia-reperfusion injury (MIRI), the joint result of ischemic injury and reperfusion injury, is associated with poor outcomes in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention. Accumulating evidence demonstrates that activated platelets directly contribute to the pathogenesis of MIRI through participating in the formation of microthrombi, interaction with leukocytes, secretion of active substances, constriction of microvasculature, and activation of spinal afferent nerves. The molecular mechanisms underlying the above detrimental effects of activated platelets include the homotypic and heterotypic interactions through surface receptors, transduction of intracellular signals, and secretion of active substances. Revealing the roles of platelet activation in MIRI and the associated mechanisms would provide potential targets/strategies for the clinical evaluation and treatment of MIRI. Further studies are needed to characterize the temporal (ischemia phase vs. reperfusion phase) and spatial (systemic vs. local) distributions of platelet activation in MIRI by multi-omics strategies. To improve the likelihood of translating novel cardioprotective interventions into clinical practice, basic researches maximally replicating the complexity of clinical scenarios would be necessary.
Keywords: Cardio-protection; Myocardial infarction; Myocardial ischemic reperfusion injury; Platelet; Platelet activation.
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