Acute myocardial infarction (AMI) is a severe condition affecting millions worldwide.During AMI, the blood supply to the heart muscle is interrupted, reducing the availability of nutrients and oxygen. Restoring blood flow is essential to save the heart muscle; paradoxically, reperfusion is not an entirely benign mechanism, and it induces reperfusion injuries.Therefore, treatments to mitigate ischemia-reperfusion (I/R) injuries are necessary. So far, there are no entirely effective pharmacological treatments to relieve I/R injuries in patients under AMI. However, pharmacological conditioning with Dexmedetomidine, a medication primarily used as a sedative and analgesic, has been reported as a promising cardioprotective agent against I/R injuries.

Due to its sedative and analgesic effects, Dexmedetomidine is a selective agonist of the alpha-2 adrenergic receptor (α2-AR) commonly used in hospitals, especially in intensive care units and surgery rooms. Although its association with cardiac protection has been suggested in previous studies, ^– the work of Chen et al.,the topic of this short editorial, delved into understanding Dexmedetomidine’s underlying mechanism of cardioprotection. Thus, in addition to demonstrating that pharmacological preconditioning with Dexmedetomidine improves cardiac function and reduces the myocardial infarct area after I/R, one of the most significant findings of this study was the relationship between Dexmedetomidine and mitophagy.

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