Evidence map›Paper›PMID 32324499›Full record

ReviewCirculation research2020

Neutrophil Extracellular Traps Participate in Cardiovascular Diseases: Recent Experimental and Clinical Insights.

Yvonne Döring, Peter Libby, Oliver Soehnlein

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 246 papers.

0numbers the graph read from it
0cells of the map it votes in
246citing papers in PubMed
15.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

246 citing papers in PubMed, 349 citations in OpenAlex.

  1. Review
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  8. Nucleic Acids as Emerging Regulators of Calcium Phosphate Biomineralization.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  9. Review
  10. Nanomaterials-Based Immunotherapy for Atherosclerosis.Small (Weinheim an der Bergstrasse, Germany) · 2026
    Review
  11. Review
  12. Article
  13. Article
  14. Review
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  16. Article
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  20. Review

186 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 3 countries.

Yvonne DöringFrom the Division of Angiology, Swiss Cardiovascular Center, Inselspital, Bern University Hospital, Switzerland (Y.D.).
Peter LibbyDivision of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA (P.L.).
Oliver SoehnleinInstitute of Cardiovascular Prevention, Department of Medicine, Ludwig-Maximilians-University Munich, Germany (Y.D., O.S.).
Brigham and Women's Hospital · USGerman Centre for Cardiovascular Research · DELudwig-Maximilians-Universität München · DE

Funding

Molecular Determinants of Arterial Remodeling in AtherogenesisR01HL080472 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LIBBY, PETER · 2005 to 2018
$5.0M
Novel mechanisms of the thrombotic complications of atherosclerosisR01HL134892 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LIBBY, PETER · 2019 to 2022
$1.7M
NHLBI NIH HHS R01 HL080472NHLBI NIH HHS R01 HL134892
6 · The paper itself

Abstract

Neutrophil extracellular traps (NETs) have recently emerged as a newly recognized contributor to venous and arterial thrombosis. These strands of DNA extruded by activated or dying neutrophils, decorated with various protein mediators, become solid-state reactors that can localize at the critical interface of blood with the intimal surface of diseased arteries and propagate and amplify the regional injury. NETs thus furnish a previously unsuspected link between inflammation, innate immunity, thrombosis, oxidative stress, and cardiovascular diseases. In response to disease-relevant stimuli, neutrophils undergo a specialized series of reactions that culminate in NET formation. DNA derived from either nuclei or mitochondria can contribute to NET formation. The DNA liberated from neutrophils forms a reticular mesh that resembles morphologically a net, rendering the acronym NETs particularly appropriate. The DNA backbone of NETs not only presents intrinsic neutrophil proteins (eg, MPO [myeloperoxidase] and various proteinases) but can gather other proteins found in blood (eg, tissue factor procoagulant). This review presents current concepts of neutrophil biology, the triggers to and mechanisms of NET formation, and the contribution of NETs to atherosclerosis and to thrombosis. We consider the use of markers of NETs in clinical studies. We aim here to integrate critically the experimental literature with the growing body of clinical information regarding NETs.

Indexed as

AnimalsArteriesAtherosclerosisBiomarkersBlood CoagulationExtracellular TrapsHumansInflammationInflammation MediatorsNeutrophilsPlaque, AtheroscleroticReactive Oxygen SpeciesRupture, SpontaneousSignal TransductionThrombosisBiomarkersInflammation MediatorsReactive Oxygen Speciesatherosclerosiscardiovascular diseasesinflammationneutrophilsthrombosis

Identifiers

PMID32324499
PMCPMC7185047
OpenAlexW3019201771

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.