The Signaling Mechanism of Remote Postconditioning of the Heart: Prospects of the Use of Remote Postconditioning for the Treatment of Acute Myocardial Infarction

Acute myocardial infarction (AMI) remains the leading cause of mortality in the world, highlighting an urgent need for the development of novel, more effective approaches for the treatment of AMI. Remote postconditioning (RPost) of the heart could be a useful approach. It was demonstrated that RPost triggers infarct size reduction, improves contractile function of the heart in reperfusion, mitigates apoptosis, and stimulates autophagy in animals with coronary artery occlusion and reperfusion. Endogenous opioid peptides and adenosine could be involved in RPost. It was found that kinases and NO-synthase participate in RPost. KATP channels, MPT pore, and STAT3 could be hypothetical end-effectors of RPost. Metabolic syndrome and old age abolish the cardioprotective effect of RPost in rats. The data on the efficacy of RPost in clinical practice are inconsistent. These data are discussed in the review.

Automated summary

Acute myocardial infarction (AMI) is the leading cause of death globally, necessitating the development of new and more effective approaches for treatment. Remote postconditioning (RPost) has shown promise in reducing infarct size, improving heart function, preventing apoptosis, and stimulating autophagy in animal models. Various mechanisms, including endogenous opioids, adenosine, kinases, and NO-synthase, may be involved in RPost. However, the efficacy of RPost in clinical practice remains inconclusive, with inconsistent results reported.