Evidence map›Paper›PMID 32673525›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2020

Neutrophil Extracellular Trap Degradation by Differently Polarized Macrophage Subsets.

Patrick Haider, Julia B Kral-Pointner, Julia Mayer, Manuela Richter, Christoph Kaun, Christine Brostjan, Wolf Eilenberg, Michael B Fischer, Walter S Speidl, Christian Hengstenberg and 3 more

Open access · hybridAbstract readComparative Study
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% 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

78 citing papers in PubMed, 1 synthesis or guideline pooled it, 111 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Macrophage Extracellular Traps in Immunity and Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Regulation of histones in thromboinflammation.Frontiers in immunology · 2026
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Islet Tissue Macrophages in Immunity Homeostasis and Type 1 Diabetes.Clinical reviews in allergy & immunology · 2025
    Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

Patrick HaiderFrom the Division of Cardiology, Department of Medicine II (P. Haider, J.B.K.-P., J.M., M.R., C.K., W.S.S., C.H., J.W., P. Hohensinner), Medical University of Vienna, Austria.
Julia B Kral-PointnerFrom the Division of Cardiology, Department of Medicine II (P. Haider, J.B.K.-P., J.M., M.R., C.K., W.S.S., C.H., J.W., P. Hohensinner), Medical University of Vienna, Austria.
Julia MayerFrom the Division of Cardiology, Department of Medicine II (P. Haider, J.B.K.-P., J.M., M.R., C.K., W.S.S., C.H., J.W., P. Hohensinner), Medical University of Vienna, Austria.
Manuela RichterFrom the Division of Cardiology, Department of Medicine II (P. Haider, J.B.K.-P., J.M., M.R., C.K., W.S.S., C.H., J.W., P. Hohensinner), Medical University of Vienna, Austria.
Christoph KaunFrom the Division of Cardiology, Department of Medicine II (P. Haider, J.B.K.-P., J.M., M.R., C.K., W.S.S., C.H., J.W., P. Hohensinner), Medical University of Vienna, Austria.
Christine BrostjanDivision of Vascular Surgery and Surgical Research Laboratories, Department of Surgery (C.B., W.E.), Medical University of Vienna, Austria.
Wolf EilenbergDivision of Vascular Surgery and Surgical Research Laboratories, Department of Surgery (C.B., W.E.), Medical University of Vienna, Austria.
Michael B FischerDepartment of Blood Group Serology and Transfusion Medicine (M.B.F.), Medical University of Vienna, Austria.
Walter S SpeidlFrom the Division of Cardiology, Department of Medicine II (P. Haider, J.B.K.-P., J.M., M.R., C.K., W.S.S., C.H., J.W., P. Hohensinner), Medical University of Vienna, Austria.
Christian HengstenbergFrom the Division of Cardiology, Department of Medicine II (P. Haider, J.B.K.-P., J.M., M.R., C.K., W.S.S., C.H., J.W., P. Hohensinner), Medical University of Vienna, Austria.
Kurt HuberWilhelminenhospital, 3rd Department of Medicine, Cardiology and Intensive Care Medicine, Vienna, Austria (K.H.).
Johann WojtaFrom the Division of Cardiology, Department of Medicine II (P. Haider, J.B.K.-P., J.M., M.R., C.K., W.S.S., C.H., J.W., P. Hohensinner), Medical University of Vienna, Austria.
Philipp HohensinnerFrom the Division of Cardiology, Department of Medicine II (P. Haider, J.B.K.-P., J.M., M.R., C.K., W.S.S., C.H., J.W., P. Hohensinner), Medical University of Vienna, Austria.
Medical University of Vienna · ATUniversität für Weiterbildung Krems · ATWilhelminen Hospital · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveMacrophages are immune cells, capable to remodel the extracellular matrix, which can harbor extracellular DNA incorporated into neutrophil extracellular traps (NETs). To study the breakdown of NETs we studied the capability of macrophage subsets to degrade these structures in vitro and in vivo in a murine thrombosis model. Furthermore, we analyzed human abdominal aortic aneurysm samples in support of our in vitro and in vivo results. Approach and Results: Macrophages were seeded onto blood clots or isolated NETs and polarized. All macrophages were capable to degrade NETs. For initial breakdown, macrophages relied on extracellular deoxyribonucleases. Proinflammatory polarization enhanced NET degradation. The boost in degradation was because of increased macropinocytosis, as inhibition by imipramine diminished their NET breakdown. Inhibition of macropinocytosis in a murine thrombosis model led to increased NET burden and reduced thrombus resolution in vivo. When analyzing abdominal aortic aneurysm samples, macrophage density furthermore corresponded negatively with the amount of local NETs in the intraluminal thrombi as well as in the vessel wall, as increased macrophage density was associated with a reduction in NET burden.

conclusionsWe provide evidence that macrophages degrade NETs by extracellular predigestion and subsequent uptake. Furthermore, we show that proinflammatory macrophages increase NET degradation through enhanced macropinocytosis, priming them for NET engulfment. Based on our findings, that inhibition of macropinocytosis in mice corresponded to increased NET amounts in thrombi and that local macrophage density in human abdominal aortic aneurysm is negatively associated with surrounding NETs, we hypothesize, that macrophages are able to degrade NETs in vivo.

Indexed as

Macrophage ActivationPinocytosisAnimalsAortic Aneurysm, AbdominalCells, CulturedDeoxyribonuclease IDeoxyribonucleasesDisease Models, AnimalEndodeoxyribonucleasesExodeoxyribonucleasesExtracellular TrapsFemaleHumansImipramineInterferon-gammaInterleukin-13Deoxyribonuclease IDeoxyribonucleasesDNASE1L1 protein, humanDNASE1L3 protein, humanDNASE2 protein, humanEndodeoxyribonucleasesExodeoxyribonucleasesImipramineInterferon-gammaInterleukin-13Interleukin-4LipopolysaccharidesMuscle ProteinsPhosphoproteinsthree prime repair exonuclease 1aortic aneurysmextracellular trapshumansmacrophagesthrombosis

Identifiers

PMID32673525
PMCPMC7447175
OpenAlexW3043284919

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.