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Epoxyeicosatrienoic acids and cardioprotection: the road to translation
Akinyemi Oni-Orisan1, Nasser Alsaleh2, Craig R Lee3
1Division of Pharmacotherapy and Experimental Therapeutics, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA; Center for Pharmacogenomics and Individualized Therapy, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Insights
Epoxyeicosatrienoic acids (EETs) show promise for treating acute myocardial infarction (AMI). Promoting EETs may offer a new therapeutic strategy to reduce cardiovascular disease burden.
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Biochemistry
Background:
- Cardiovascular diseases, including acute myocardial infarction (AMI), are a major global health concern, driving significant morbidity and mortality.
- Existing treatments for AMI are established, yet there is a critical need for novel therapeutics to prevent disease progression and reduce the global health burden.
- Epoxyeicosatrienoic acids (EETs), cytochrome P450-derived epoxyeicosanoids, are emerging as key players in cardiovascular protection.
Purpose of the Study:
- To review the potential clinical utility of promoting epoxyeicosatrienoic acids (EETs) as a therapeutic strategy for acute myocardial infarction (AMI).
- To explore the cardioprotective effects and underlying mechanisms of EETs in preclinical AMI models, focusing on ischemia-reperfusion injury.
- To examine human cohort studies linking EETs and related pathways to coronary artery disease risk and identify areas for further clinical investigation.
Main Methods:
- Review of preclinical studies detailing the cardioprotective effects of EETs in models of AMI and myocardial ischemia-reperfusion injury.
- Analysis of human cohort studies investigating the association between EET levels, related pathways, and coronary artery disease risk.
- Identification of knowledge gaps and future research directions for clinical translation of EET-based therapies for AMI.
Main Results:
- Preclinical evidence strongly supports the cardioprotective role of EETs, particularly in mitigating myocardial ischemia-reperfusion injury.
- Human studies suggest a correlation between EETs, associated signaling pathways, and the risk of developing coronary artery disease.
- The review highlights the need for further translational research to bridge the gap between preclinical findings and clinical application.
Conclusions:
- Epoxyeicosatrienoic acids (EETs) represent a promising therapeutic target for acute myocardial infarction (AMI).
- Promoting EETs' cardiovascular effects holds potential for a novel clinical strategy to combat AMI consequences.
- Further investigation is crucial to translate the existing evidence into effective clinical treatments for AMI.
Abstract:
Cardiovascular disease, including acute myocardial infarction (AMI), is the leading cause of morbidity and mortality globally, despite well-established treatments. The discovery and development of novel therapeutics that prevent the progression of devastating consequences following AMI are thus important in reducing the global burden of this devastating disease. Scientific evidence for the protective effects of epoxyeicosatrienoic acids (EETs) in the cardiovascular system is rapidly emerging and suggests that promoting the effects of these cytochrome P450-derived epoxyeicosanoids is a potentially viable clinical therapeutic strategy. Through a translational lens, this review will provide insight into the potential clinical utility of this therapeutic strategy for AMI by 1) outlining the known cardioprotective effects of EETs and underlying mechanisms demonstrated in preclinical models of AMI with a particular focus on myocardial ischemia-reperfusion injury, 2) describing studies in human cohorts that demonstrate a relationship between EETs and associated pathways with coronary artery disease risk, and 3) discussing preclinical and clinical areas that require further investigation in order to increase the probability of successfully translating this rapidly emerging body of evidence into a clinically applicable therapeutic strategy for AMI.
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