ArticlePeerJ2023
Neutrophil extracellular trap burden correlates with the stenosis of coronary atherosclerosis.
Article in PeerJ, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Neutrophil extracellular traps in cardiovascular disease: Mechanisms and therapeutic implications (Review).International journal of molecular medicine · 2026Review
- Association between neutrophil extracellular traps, the Von Willebrand factor axis, and clinical outcome in stable coronary artery disease.Frontiers in cardiovascular medicine · 2026Article
- A comprehensive phenome wide analysis of the role of neutrophils in health and disease.Journal of leukocyte biology · 2025Article
- NETosis in myocardial ischemia-reperfusion injury: From mechanisms to therapies (Review).Biomedical reports · 2025Review
- Novel Circulating Biomarkers in Aortic Valve Stenosis.International journal of molecular sciences · 2025Review
- Neutrophil extracellular traps in homeostasis and disease.Signal transduction and targeted therapy · 2024Review
- Myeloid Cells in Myocardial Ischemic Injury: The Role of the Macrophage Migration Inhibitory Factor.Life (Basel, Switzerland) · 2024Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Coronary atherosclerosis diseases (CADs) are associated with chronic inflammation. Neutrophil extracellular traps (NETs) are a type of novel proinflammatory cytokines whose levels are dramatically elevated in acute coronary syndrome. We conducted this study to further evaluate the association between circulating NET-associated markers and CAD in Chinese adults. Methods: A total of 174 patients with CAD and 55 healthy controls were screened using percutaneous coronary intervention or coronary computed tomography angiography. Blood lipid levels, blood glucose levels, and blood cell counts were determined using commercial kits. Serum levels of myeloperoxidase (MPO) and neutrophil elastase (NE) were measured using ELISA. Double-stranded DNA (dsDNA) in serum was quantified using the Quant-iT PicoGreen assay. We also compared the circulating NET levels with various parameters in the study subjects. Results: The levels of serum NET markers, dsDNA, MPO, and NE, were significantly elevated in patients with CAD, particularly in the severe group, consistent with the increase in neutrophil counts. The levels of NET markers correlated with the risk factors of AS, increasing with the number of risk factors. NET markers were identified as independent risk factors for severe coronary stenosis and also as predictors of severe CAD. Conclusion: NETs may be related to AS and serve as indicators or predictors of stenosis in patients with severe CAD.
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Identifiers
What OpenQuestion holds
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.