Evidence map›Paper›PMID 31481482›Full record

ArticleBlood2019

Eosinophil-platelet interactions promote atherosclerosis and stabilize thrombosis with eosinophil extracellular traps.

Charlotte Marx, Julia Novotny, Danby Salbeck, Katie R Zellner, Leo Nicolai, Kami Pekayvaz, Badr Kilani, Sven Stockhausen, Niklas Bürgener, Danny Kupka and 12 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
118citing papers in PubMed, 3 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

118 citing papers in PubMed, 3 syntheses or guidelines pooled it, 203 citations in OpenAlex.

  1. Guideline
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Article
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  18. Coronary artery disease and cancer: Shared risk factors, pathogenesis, and treatment effects.American heart journal plus : cardiology research and practice · 2026
    Review
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58 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors at 7 institutions in 5 countries.

Charlotte MarxMedizinische Klinik und Poliklinik I, Ludwig-Maximilians-Universität, Munich, Germany.
Julia NovotnyMedizinische Klinik und Poliklinik I, Ludwig-Maximilians-Universität, Munich, Germany.
Danby SalbeckMedizinische Klinik und Poliklinik I, Ludwig-Maximilians-Universität, Munich, Germany.
Katie R ZellnerDivision of Pulmonary Medicine, Department of Biochemistry and Molecular Biology, Mayo Clinic Arizona, Scottsdale, AZ.
Leo NicolaiMedizinische Klinik und Poliklinik I, Ludwig-Maximilians-Universität, Munich, Germany.
Kami PekayvazMedizinische Klinik und Poliklinik I, Ludwig-Maximilians-Universität, Munich, Germany.
Badr KilaniMedizinische Klinik und Poliklinik I, Ludwig-Maximilians-Universität, Munich, Germany.
Sven StockhausenMedizinische Klinik und Poliklinik I, Ludwig-Maximilians-Universität, Munich, Germany.
Niklas BürgenerMedizinische Klinik und Poliklinik I, Ludwig-Maximilians-Universität, Munich, Germany.
Danny KupkaMedizinische Klinik und Poliklinik I, Ludwig-Maximilians-Universität, Munich, Germany.
Thomas J StockerMedizinische Klinik und Poliklinik I, Ludwig-Maximilians-Universität, Munich, Germany.
Ludwig T WeckbachMedizinische Klinik und Poliklinik I, Ludwig-Maximilians-Universität, Munich, Germany.
Joachim PircherMedizinische Klinik und Poliklinik I, Ludwig-Maximilians-Universität, Munich, Germany.
Markus MoserDepartment of Molecular Medicine, Max Planck Institute of Biochemistry, Martinsried, Germany.
Michael JonerGerman Center for Cardiovascular Research, partner site Munich Heart Alliance, Munich, Germany.
Walter DesmetDepartment of Cardiology, University Hospital Leuven, Leuven, Belgium.
Tom AdriaenssensDepartment of Cardiology, University Hospital Leuven, Leuven, Belgium.
Franz-Josef NeumannUniversitäts-Herzzentrum Freiburg, Bad Krozingen, Germany.
Anthony H GerschlickDepartment of Cardiovascular Sciences, University of Leicester and Leicester National Institute for Health Research Cardiovascular Biomedical Research Unit, Glenfield Hospital, Leicester, United Kingdom; and.
Jurrien M Ten BergDepartment of Cardiology, St. Antonius Hospital, Nieuwegein, The Netherlands.
Michael LorenzMedizinische Klinik und Poliklinik I, Ludwig-Maximilians-Universität, Munich, Germany.
Konstantin StarkMedizinische Klinik und Poliklinik I, Ludwig-Maximilians-Universität, Munich, Germany.
German Centre for Cardiovascular Research · DEKU Leuven · BEMayo Clinic in Arizona · USSt. Antonius Ziekenhuis · NLTUM Klinikum · DEUniversitäts-Herzzentrum Freiburg-Bad Krozingen · DEUniversity of Leicester · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clinical observations implicate a role of eosinophils in cardiovascular diseases because markers of eosinophil activation are elevated in atherosclerosis and thrombosis. However, their contribution to atherosclerotic plaque formation and arterial thrombosis remains unclear. In these settings, we investigated how eosinophils are recruited and activated through an interplay with platelets. Here, we provide evidence for a central importance of eosinophil-platelet interactions in atherosclerosis and thrombosis. We show that eosinophils support atherosclerotic plaque formation involving enhanced von Willebrand factor exposure on endothelial cells and augmented platelet adhesion. During arterial thrombosis, eosinophils are quickly recruited in an integrin-dependent manner and engage in interactions with platelets leading to eosinophil activation as we show by intravital calcium imaging. These direct interactions induce the formation of eosinophil extracellular traps (EETs), which are present in human thrombi and constitute a substantial part of extracellular traps in murine thrombi. EETs are decorated with the granule protein major basic protein, which causes platelet activation by eosinophils. Consequently, targeting of EETs diminished thrombus formation in vivo, which identifies this approach as a novel antithrombotic concept. Finally, in our clinical analysis of coronary artery thrombi, we identified female patients with stent thrombosis as the population that might derive the greatest benefit from an eosinophil-inhibiting strategy. In summary, eosinophils contribute to atherosclerotic plaque formation and thrombosis through an interplay with platelets, resulting in mutual activation. Therefore, eosinophils are a promising new target in the prevention and therapy of atherosclerosis and thrombosis.

Indexed as

AnimalsAtherosclerosisBlood PlateletsEosinophilsExtracellular TrapsHumansMiceMice, Inbred C57BLMice, TransgenicPlatelet ActivationThrombosis

Identifiers

PMID31481482
PMCPMC6908806
OpenAlexW2972038129

What OpenQuestion holds

Textmetadata
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.