ArticleEuropean heart journal2025
Malondialdehyde-specific natural IgM inhibit NETosis triggered by culprit site-derived extracellular vesicles from myocardial infarction patients.
Article in European heart journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Extracellular Vesicles in Cardiovascular Disease: Intercellular Signaling, Liquid Biopsy Biomarkers, and Therapeutic Translation.Circulation research · 2026Review
- Malondialdehyde epitopes exposed on dying cells are potent modulators of complement activity and efferocytosis.Journal of lipid research · 2026Article
- NET-DNA Activates the ANXA2/TMEM215/BiP Axis to Promote Mitophagy-Mediated Anoikis Resistance in Endometriosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The systemic immune-inflammation index in coronary heart disease: a narrative review of thromboinflammation, phenotype-dependent utility, and clinical translation.Frontiers in cardiovascular medicine · 2026Review
- A malondialdehyde-activated fluorescent probe reveals lysosomal dysfunction in atherosclerosis.Chemical science · 2025Article
- Extracellular vesicles in cardiovascular diseases: pathogenic mediators, diagnostic tools, and therapeutic vectors.Frontiers in cardiovascular medicine · 2025Review
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20 authors.
Funding
Abstract
BACKGROUND AND
aimsNeutrophil extracellular traps (NETs) trigger atherothrombosis during acute myocardial infarction (AMI), but mechanisms of induction remain unclear. Levels of extracellular vesicles (EV) carrying oxidation-specific epitopes (OSE), which are targeted by specific natural immunoglobulin M (IgM), are increased at the culprit site in AMI. This study investigated EV as inducers of NETosis and assessed the inhibitory effect of natural anti-OSE-IgM in this process.
methodsBlood from the culprit and peripheral site of ST-segment elevation myocardial infarction (STEMI) patients (n = 28) was collected, and myocardial function assessed by cardiac magnetic resonance imaging (cMRI) 4 ± 2 days and 195 ± 15 days post-AMI. Extracellular vesicles were isolated from patient plasma and cell culture supernatants for neutrophil stimulation in vitro and in vivo, in the presence of a malondialdehyde (MDA)-specific IgM or an isotype control. NETosis and neutrophil functions were assessed via enzyme-linked immunosorbent assay and fluorescence microscopy. Pharmacological inhibitors were used to map signalling pathways. Neutrophil extracellular trap markers and anti-OSE-IgM were measured by ELISA.
resultsCD45+ MDA+ EV and NET markers were elevated at the culprit site. Extracellular vesicles induced neutrophil activation and NET formation via TLR4 and PAD4, and mice injected with EV showed increased NETosis. Malondialdehyde-specific IgM levels were inversely associated with citH3 in STEMI patient blood. An MDA-specific IgM inhibited EV-induced NET release in vitro and in vivo. CD45+ MDA+ EV concentrations inversely correlated with left ventricular ejection fraction post-AMI.
conclusionsCulprit site-derived EV induce NETosis, while MDA-specific natural IgM inhibit this effect, potentially impacting outcome after AMI.
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