ArticleScientific reports2019
Neutrophil extracellular traps and monocyte subsets at the culprit lesion site of myocardial infarction patients.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.
- Neutrophil-Enriched Biomarkers and Long-Term Prognosis in Acute Coronary Syndrome: a Systematic Review and Meta-analysis.Journal of cardiovascular translational research · 2024Pooled it
- Cardiac repair after myocardial infarction: A two-sided role of inflammation-mediated.Frontiers in cardiovascular medicine · 2022Pooled it
- Neutrophil extracellular traps in cardiovascular disease: Mechanisms and therapeutic implications (Review).International journal of molecular medicine · 2026Review
- Spatiotemporal Nanotherapy After Myocardial Infarction: Targeting the Inflammatory-to-reparative Transition With Extracellular Vesicles and Engineered Nanoparticles.Cardiovascular drugs and therapy · 2026Review
- Review
- Article
- Circulating Markers of Neutrophil Extracellular Traps for Long-Term Prognosis in Patients With Acute Chest Pain.Journal of the American Heart Association · 2026Article
- Diagnostic Value of Serum CXCL2 and Fibronectin-1 in Acute Myocardial Infarction and Their Association with Neutrophil Extracellular Trap Formation.International journal of general medicine · 2026Article
- NETosis in myocardial ischemia-reperfusion injury: From mechanisms to therapies (Review).Biomedical reports · 2025Review
- Multifaceted roles of neutrophils in cardiac disease.Journal of leukocyte biology · 2025Review
- Inflammatory Cell-Targeted Delivery Systems for Myocardial Infarction Treatment.Bioengineering (Basel, Switzerland) · 2025Review
- Design of a Robust Flow Cytometric Approach for Phenotypical and Functional Analysis of Human Monocyte Subsets in Health and Disease.Biomolecules · 2024Article
- Myeloid Cells in Myocardial Ischemic Injury: The Role of the Macrophage Migration Inhibitory Factor.Life (Basel, Switzerland) · 2024Review
- Pan-Immune-Inflammatory Value is Superior to Other Inflammatory Indicators in Predicting Inpatient Major Adverse Cardiovascular Events and Severe Coronary Artery Stenosis after Percutaneous Coronary Intervention in STEMI Patients.Reviews in cardiovascular medicine · 2024Article
- A secreted sirtuin fromScience advances · 2023Article
- Prognostic Significance of Activated Monocytes in Patients with ST-Elevation Myocardial Infarction.International journal of molecular sciences · 2023Article
- Molecular and cellular pathophysiology of circulating cardiomyocyte-specific cell free DNA (cfDNA): Biomarkers of heart failure and potential therapeutic targets.Genes & diseases · 2023Review
- Circulating neutrophil extracellular traps in cats with hypertrophic cardiomyopathy and cardiogenic arterial thromboembolism.Journal of veterinary internal medicine · 2023Article
- Impact of Reperfusion on Temporal Immune Cell Dynamics After Myocardial Infarction.Journal of the American Heart Association · 2023Review
- Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neutrophils release their chromatin into the extracellular space upon activation. These web-like structures are called neutrophil extracellular traps (NETs) and have potent prothrombotic and proinflammatory properties. In ST-elevation myocardial infarction (STEMI), NETs correlate with increased infarct size. The interplay of neutrophils and monocytes impacts cardiac remodeling. Monocyte subsets are classified as classical, intermediate and non-classical monocytes. In the present study, in vitro stimulation with NETs led to an increase of intermediate monocytes and reduced expression of CX3CR1 in all subsets. Intermediate monocytes have been associated with poor outcome, while non-classical CX3CR1-positive monocytes could have reparative function after STEMI. We characterized monocyte subsets and NET markers at the culprit lesion site of STEMI patients (n = 91). NET surrogate markers were increased and correlated with larger infarct size and with fewer non-classical monocytes. Intermediate and especially non-classical monocytes were increased at the culprit site compared to the femoral site. Low CX3CR1 expression of monocytes correlated with high NET markers and increased infarct size. In this translational system, causality cannot be proven. However, our data suggest that NETs interfere with monocytic differentiation and receptor expression, presumably promoting a subset shift at the culprit lesion site. Reduced monocyte CX3CR1 expression may compromise myocardial salvage.
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Registered trials
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