Evidence map›Paper›PMID 31315434›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2019

Neutrophil Extracellular Traps: Villains and Targets in Arterial, Venous, and Cancer-Associated Thrombosis

Charlotte Thålin, Yohei Hisada, Staffan Lundström, Nigel Mackman, Håkan Wallén

Open access · greenAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 256 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
256citing papers in PubMed, 1 pooled it
17.1field-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

256 citing papers in PubMed, 1 synthesis or guideline pooled it, 385 citations in OpenAlex.

  1. Pooled it
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  11. Neutrophil extracellular traps (NETosis) in gynecologic cancers: from pathogenesis to therapeutic opportunities: a narrative review.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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196 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

5 authors at 2 institutions in 2 countries.

Charlotte ThålinFrom the Division of Internal Medicine, Department of Clinical Sciences, Danderyd Hospital (C.T.), Karolinska Institutet, Stockholm, Sweden.
Yohei HisadaDivision of Hematology and Oncology, Department of Medicine, University of North Carolina at Chapel Hill (Y.H., N.M.).
Staffan LundströmDepartment of Oncology-Pathology (S.L.), Karolinska Institutet, Stockholm, Sweden.
Nigel MackmanDivision of Hematology and Oncology, Department of Medicine, University of North Carolina at Chapel Hill (Y.H., N.M.).
Håkan WallénDivision of Cardiovascular Medicine (H.W.), Karolinska Institutet, Stockholm, Sweden.
Karolinska Institutet · SEUniversity of North Carolina at Chapel Hill · US

Funding

Research Training in Hematology at UNC Chapel HillT32HL007149 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Nigel S. Key · 1985 to 2026
$8.6M
NHLBI NIH HHS T32 HL007149
6 · The paper itself

Abstract

Recent studies have demonstrated a role of neutrophils in both venous and arterial thrombosis. A key prothrombotic feature of neutrophils is their ability to release web-like structures composed of DNA filaments coated with histones and granule proteins referred to as neutrophil extracellular traps (NETs). NETs were discovered over a decade ago as part of our first line of host defense against invading microorganisms. Although NETs have a protective role against pathogens, recent data suggest that an uncontrolled and excessive NET formation within the vasculature may contribute to pathological thrombotic disorders. In vitro studies suggest that NETs promote vessel occlusion by providing a scaffold for platelets, red blood cells, extracellular vesicles, and procoagulant molecules, such as von Willebrand factor and tissue factor. In addition, NET components enhance coagulation by both activating the intrinsic pathway and degrading an inhibitor of the extrinsic pathway (tissue factor pathway inhibitor). NET formation has, therefore, been proposed to contribute to thrombus formation and propagation in arterial, venous, and cancer-associated thrombosis. This review will describe animal and human studies suggesting a role of NETs in the pathogenesis of various thrombotic disorders. Targeting NETs may be a novel approach to reduce thrombosis without affecting hemostasis.

Indexed as

AnimalsAtherosclerosisChromatinDeoxyribonuclease IExtracellular TrapsHumansNeoplasmsNeutrophilsThrombosisVenous ThrombosisChromatinDeoxyribonuclease Iextracellular trapsextracellular vesicleshistonesneutrophilsthrombosis

Identifiers

PMID31315434
PMCPMC6703916
OpenAlexW2963080746

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.