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Published on: November 3, 2023
Past and present course of cardioprotection against ischemia-reperfusion injury
David A Liem1, Henry M Honda, Jun Zhang
1Department of Physiology, Division of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Insights
Cardioprotection research explores how to limit heart damage from ischemia-reperfusion injury. Recent studies focus on signaling pathways and mitochondrial protection during reperfusion to salvage heart tissue.
Area of Science:
- Cardiovascular Research
- Myocardial Ischemia-Reperfusion Injury
Background:
- Ischemic heart disease is a leading cause of mortality globally.
- Direct interventions to reduce infarct size during acute myocardial infarction have yielded disappointing results.
- Ischemic preconditioning and postconditioning demonstrate consistent cardioprotective effects in experimental models.
Observation:
- Research has increasingly focused on intracellular signaling pathways involved in preconditioning and postconditioning.
- The reperfusion injury salvage kinases (RISK) pathway, including protein kinase B and extracellular signal-regulated kinases, shows potential for cardioprotection.
- Inhibition of mitochondrial permeability transition during reperfusion is also a promising cardioprotective strategy.
Findings:
- Activation of RISK pathway components during postischemic reperfusion can induce cardioprotection.
- Targeting mitochondrial permeability transition offers a strong cardioprotective effect against ischemia-reperfusion injury.
- This review summarizes historical and current research on cardioprotection against myocardial I/R injury.
Implications:
- Understanding these pathways and targets could lead to novel therapeutic strategies for myocardial infarction.
- Future research may focus on translating these findings into clinical applications to improve patient outcomes.
- Developing effective treatments for ischemia-reperfusion injury remains a critical goal in cardiovascular medicine.
Abstract:
Despite tremendous advances in cardiovascular research and clinical therapy, ischemic heart disease remains the leading cause of serious morbidity and mortality in western society and is growing in developing countries. For the past 5 decades, many scientists have studied the pathophysiology of myocardial ischemia-reperfusion (I/R) injury leading to infarction. With the exception of reperfusion therapy, attempts to salvage the myocardium during an acute myocardial infarction showed disappointing results in directly decreasing infarct size. Nevertheless, the phenomena of ischemic preconditioning and ischemic postconditioning show a consistent and robust cardioprotective effect in every used experimental animal model. As a result, many studies have focused on the intracellular protective signaling pathways that are involved in preconditioning and postconditioning. More recently, it has been suggested that components of the reperfusion injury salvage kinases pathway, protein kinase B, and the extracellular signal-regulated kinases can induce cardioprotection against I/R injury when they are activated during the postischemic reperfusion period. In addition, inhibition of mitochondrial permeability transition during postischemic reperfusion also shows a strong cardioprotective effect against I/R injury. The present mini-review highlights a short summary of the historical and present course of research into cardioprotection against myocardial I/R injury.
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