ArticleCardiovascular research2019
Reduction of myocardial ischaemia-reperfusion injury by inactivating oxidized phospholipids.
Article in Cardiovascular research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 87 citations in OpenAlex.
- Lipoprotein(a) and oxidized phospholipids are associated with myocardial inflammation after acute myocardial infarction.Nature cardiovascular research · 2026Trial
- Neutralization of pathogenic PC-OxPL by AAV-delivered scFv as a therapeutic strategy for amyotrophic lateral sclerosis.Molecular therapy. Advances · 2026Article
- Oxidized Phospholipids Aggravate Hepatic Ischemia/Reperfusion Injury by Promoting Macrophage M1 Polarization Via Regulating the Wnt/β-catenin/Autophagy Axis.Inflammation · 2026Article
- Impact of Oxidized Phospholipids on Outcomes from Cerebral Ischemia and Reperfusion Injury.Pharmaceutics · 2026Article
- Glutathione Synthesis via the Cystine/Glutamate Transporter Promotes the Formation of Tertiary Lymphoid Structures in the Kidney.Journal of the American Society of Nephrology : JASN · 2026Article
- Oxidized phosphatidylcholines deposition drives chronic neurodegeneration in a mouse model of progressive multiple sclerosis via IL-1β signaling.Nature neuroscience · 2026Article
- Structural Insights into Recognition and Translocation of Oxidized Phospholipid by CD36 Using Mass Spectrometry, Molecular Docking, Dynamics, and Metadynamics Simulations.Journal of the American Chemical Society · 2025Article
- Oxidized phosphatidylcholines activate NOX1-mediated oxidative stress response and shift glucose metabolism in cardiac cells.American journal of physiology. Cell physiology · 2025Article
- Unveiling biomarkers via plasma metabolome profiling for diabetic macrovascular and microvascular complications.Cardiovascular diabetology · 2025Article
- Unleashing the potential of exercise: conquering cardiovascular disease by targeting inflammasome activation.European journal of medical research · 2025Review
- An Immune Assay to Quantify the Neutralization of Oxidation-Specific Epitopes by Human Blood Plasma.Antioxidants (Basel, Switzerland) · 2025Article
- Plasma levels of anti phosphocholine IgM antibodies are negatively correlated with bone mineral density in humans.Scientific reports · 2025Article
- Article
- Lipoprotein(a), Oxidized Phospholipids, and Progression to Symptomatic Heart Failure: The CASABLANCA Study.Journal of the American Heart Association · 2024Article
- Oxidized phospholipids in cardiovascular disease.Nature reviews. Cardiology · 2024Review
- Deciphering ferroptosis in critical care: mechanisms, consequences, and therapeutic opportunities.Frontiers in immunology · 2024Review
- Single chain fragment variable, a new theranostic approach for cardiovascular diseases.Frontiers in immunology · 2024Review
- Mitochondrial Regulation of Ferroptosis in Cancer Therapy.International journal of molecular sciences · 2023Review
- Phospholipids, the Masters in the Shadows during Healing after Acute Myocardial Infarction.International journal of molecular sciences · 2023Review
- Zooming in and out of ferroptosis in human disease.Frontiers of medicine · 2023Review
Corrections and comments
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Authors and funding
22 authors at 4 institutions in 3 countries.
Funding
Abstract
Aims: Myocardial ischaemia followed by reperfusion (IR) causes an oxidative burst resulting in cellular dysfunction. Little is known about the impact of oxidative stress on cardiomyocyte lipids and their role in cardiac cell death. Our goal was to identify oxidized phosphatidylcholine-containing phospholipids (OxPL) generated during IR, and to determine their impact on cell viability and myocardial infarct size. Methods and results: OxPL were quantitated in isolated rat cardiomyocytes using mass spectrophotometry following 24 h of IR. Cardiomyocyte cell death was quantitated following exogenously added OxPL and in the absence or presence of E06, a 'natural' murine monoclonal antibody that binds to the PC headgroup of OxPL. The impact of OxPL on mitochondria in cardiomyocytes was also determined using cell fractionation and Bnip expression. Transgenic Ldlr-/- mice, overexpressing a single-chain variable fragment of E06 (Ldlr-/--E06-scFv-Tg) were used to assess the effect of inactivating endogenously generated OxPL in vivo on myocardial infarct size. Following IR in vitro, isolated rat cardiomyocytes showed a significant increase in the specific OxPLs PONPC, POVPC, PAzPC, and PGPC (P < 0.05 to P < 0.001 for all). Exogenously added OxPLs resulted in significant death of rat cardiomyocytes, an effect inhibited by E06 (percent cell death with added POVPC was 22.6 ± 4.14% and with PONPC was 25.3 ± 3.4% compared to 8.0 ± 1.6% and 6.4 ± 1.0%, respectively, with the addition of E06, P < 0.05 for both). IR increased mitochondrial content of OxPL in rat cardiomyocytes and also increased expression of Bcl-2 death protein 3 (Bnip3), which was inhibited in presence of E06. Notably cardiomyocytes with Bnip3 knock-down were protected against cytotoxic effects of OxPL. In mice exposed to myocardial IR in vivo, compared to Ldlr-/- mice, Ldlr-/--E06-scFv-Tg mice had significantly smaller myocardial infarct size normalized to area at risk (72.4 ± 21.9% vs. 47.7 ± 17.6%, P = 0.023). Conclusions: OxPL are generated within cardiomyocytes during IR and have detrimental effects on cardiomyocyte viability. Inactivation of OxPL in vivo results in a reduction of infarct size.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.