ArticleCirculation2024
Novel Role for Cardiolipin as a Target of Therapy to Mitigate Myocardial Injury Caused by Venoarterial Extracorporeal Membrane Oxygenation.
Article in Circulation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Lipid Cargo of Small Extracellular Vesicles as a Novel Contributor to Cardiovascular Diseases.International journal of molecular sciences · 2026Review
- LipiDecipher: A Structure-Oriented Analytical Framework for Interpretable Clinical Lipidomics.Metabolites · 2026Article
- A novel evaluation indicator for pediatric fulminant myocarditis: diagnostic and prognostic value of the HALP score.BMC pediatrics · 2026Article
- Mitochondria-targeted nanotechnology in cardiovascular diseases: a review of recent advances.Regenerative biomaterials · 2026Review
- Exploring the effects of moxibustion on pathological remodeling in rats with myocardial ischemia-reperfusion injury based on mitochondrial cardiolipin protection.Frontiers in pharmacology · 2026Article
- Uncovering mitochondrial dynamics-related genes as potential diagnostic biomarkers for acute myocardial infarction.Frontiers in cardiovascular medicine · 2026Article
- Normoxemic Extracorporeal Membrane Oxygenation Reduces Infarct Size and Preserves Mitochondrial Integrity in Preclinical Models of Acute Myocardial Infarction.Journal of cardiovascular translational research · 2025Article
- Cardiac rehabilitation in porcine models: Advances in therapeutic strategies for ischemic heart disease.Zoological research · 2025Review
- Metabolic anomalies in vitiligo: a new frontier for drug repurposing strategies.Frontiers in pharmacology · 2025Article
- Myocardial Recovery in Cardiogenic Shock.Methodist DeBakey cardiovascular journal · 2024Review
Corrections and comments
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Authors and funding
19 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundCardiolipin is a mitochondrial-specific phospholipid that maintains integrity of the electron transport chain (ETC) and plays a central role in myocardial ischemia/reperfusion injury. Tafazzin is an enzyme that is required for cardiolipin maturation. Venoarterial extracorporeal membrane oxygenation (VA-ECMO) use to provide hemodynamic support for acute myocardial infarction has grown exponentially, is associated with poor outcomes, and is under active clinical investigation, yet the mechanistic effect of VA-ECMO on myocardial damage in acute myocardial infarction remains poorly understood. We hypothesized that VA-ECMO acutely depletes myocardial cardiolipin and exacerbates myocardial injury in acute myocardial infarction.
methodsWe examined cardiolipin and tafazzin levels in human subjects with heart failure and healthy swine exposed to VA-ECMO and used a swine model of closed-chest myocardial ischemia/reperfusion injury to evaluate the effect of VA-ECMO on cardiolipin expression, myocardial injury, and mitochondrial function.
resultsCardiolipin and tafazzin levels are significantly reduced in the left ventricles of individuals requiring VA-ECMO compared with individuals without VA-ECMO before heart transplantation. Six hours of exposure to VA-ECMO also decreased left ventricular levels of cardiolipin and tafazzin in healthy swine compared with sham controls. To explore whether cardiolipin depletion by VA-ECMO increases infarct size, we performed left anterior descending artery occlusion for a total of 120 minutes followed by 180 minutes of reperfusion in adult swine in the presence and absence of MTP-131, an amphipathic molecule that interacts with cardiolipin to stabilize the inner mitochondrial membrane. Compared with reperfusion alone, VA-ECMO activation beginning after 90 minutes of left anterior descending artery occlusion increased infarct size (36±8% versus 48±7%;
conclusionsWe identified a novel mechanism by which VA-ECMO promotes myocardial injury and further identify cardiolipin as an important target of therapy to reduce infarct size and to preserve mitochondrial function in the setting of VA-ECMO for acute myocardial infarction.
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