ArticleBasic research in cardiology2019
Neutrophil extracellular traps and fibrocytes in ST-segment elevation myocardial infarction.
Article in Basic research in cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 85 citations in OpenAlex.
- Tocilizumab increases citrullinated histone 3 in non-ST segment elevation myocardial infarction.Open heart · 2021Trial
- Neutrophil extracellular trap components and myocardial recovery in post-ischemic acute heart failure.PloS one · 2020Trial
- Neutrophil extracellular traps in cardiovascular disease: Mechanisms and therapeutic implications (Review).International journal of molecular medicine · 2026Review
- Review
- Reduced ALDH2 Activity and Cardiovascular Carbonyl Stress: From Reactive Aldehyde Networks to Coronary Microvascular Obstruction.Cardiovascular toxicology · 2026Review
- Cardiac immunity and heart repair: Mechanism, challenge, and future direction.Chinese medical journal · 2026Review
- AlEuropean journal of nuclear medicine and molecular imaging · 2026Article
- Extracellular Traps in Coronary Thrombus Aspirates from Patients with ST-Elevation Myocardial Infarction.International journal of molecular sciences · 2026Article
- Review
- Neutrophil extracellular traps in post-traumatic urethral microenvironment promote hypertrophic urethral stricture via the TLR9/NF-kB/Smad3/IL-8 axis.Apoptosis : an international journal on programmed cell death · 2026Article
- Clinical and Biomarker Predictors of Adverse Left Ventricular Remodeling After First STEMI: Insights into Phenotype Variability Using CMR.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Circulating Markers of Neutrophil Extracellular Traps for Long-Term Prognosis in Patients With Acute Chest Pain.Journal of the American Heart Association · 2026Article
- Heart failure in old hypertensive rats is accompanied by the increase of neutrophil extracellular traps and myeloid-derived suppressor cells.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Inflammatory responses driven by neutrophil extracellular traps in cardiovascular diseases: molecular mechanisms, emerging biomarkers, and therapeutic targets.Frontiers in immunology · 2026Review
- A NET-associated immunothrombotic phenotype is associated with coronary no-reflow and myocardial injury after primary PCI in ST-segment elevation myocardial infarction: a real-world translational cohort.Frontiers in immunology · 2026Article
- Neutrophil Extracellular Traps Activate Meningeal Fibroblast to Aggravate Subarachnoid Fibrosis in Kaolin-Induced Hydrocephalus in Rats.Immunity, inflammation and disease · 2025Article
- Neutrophil Extracellular Traps in Cardiovascular Diseases: Pathological Roles and Therapeutic Implications.Biomolecules · 2025Review
- The Immune Microenvironment: New Therapeutic Implications in Organ Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Colchicine Attenuates Microvascular Obstruction after Myocardial Ischemia-Reperfusion Injury by Inhibiting the Proliferation of Neutrophil in Bone Marrow.Cardiovascular drugs and therapy · 2025Article
- Prognostic Role of Pan-Immune-Inflammatory Value in Patients with Non-ST-Segment Elevation Acute Coronary Syndrome.Journal of cardiovascular development and disease · 2025Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leukocyte-mediated inflammation is central in atherothrombosis and ST-segment elevation myocardial infarction (STEMI). Neutrophil extracellular traps (NETs) have been shown to enhance atherothrombosis and stimulate fibroblast function. We analyzed the effects of NETs on cardiac remodeling after STEMI. We measured double-stranded (ds)DNA and citrullinated histone H3 (citH3) as NET surrogate markers in human culprit site and femoral blood collected during primary percutaneous coronary intervention (n = 50). Fibrocytes were characterized in whole blood by flow cytometry, and in culprit site thrombi and myocardium by immunofluorescence. To investigate mechanisms of fibrocyte activation, isolated NETs were used to induce fibrocyte responses in vitro. Enzymatic infarct size was assessed using creatine-phosphokinase isoform MB area under the curve. Left ventricular function was measured by transthoracic echocardiography. NET surrogate markers were increased at the culprit site compared to the femoral site and were positively correlated with infarct size and left ventricular dysfunction at follow-up. In vitro, NETs promoted fibrocyte differentiation from monocytes and induced fibrocyte activation. Highly activated fibrocytes accumulated at the culprit site and in the infarct transition zone. Our data suggest that NETs might be important mediators of fibrotic remodeling after STEMI, possibly by stimulating fibrocytes.
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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.