Evidence map›Paper›PMID 35174225›Full record

ReviewFrontiers in cardiovascular medicine2021

Neutrophil-Platelet Interactions as Novel Treatment Targets in Cardiovascular Disease.

Rainer Kaiser, Raphael Escaig, Johanna Erber, Leo Nicolai

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cardiovascular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 71 citations in OpenAlex.

  1. Observational
  2. Review
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  15. Beyond Killing: The Overlooked Contribution of Neutrophils to Tissue Repair.International journal of molecular sciences · 2025
    Review
  16. Article
  17. Article
  18. Role of platelets and NETs in arterial thrombosis.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  19. Multifaceted roles of neutrophils in cardiac disease.Journal of leukocyte biology · 2025
    Review
  20. Review
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

4 authors at 3 institutions in 1 country.

Rainer KaiserDepartment of Medicine I, University Hospital, Ludwig-Maximilians University Munich, Munich, Germany.
Raphael EscaigDepartment of Medicine I, University Hospital, Ludwig-Maximilians University Munich, Munich, Germany.
Johanna ErberDepartment of Internal Medicine II, School of Medicine, University Hospital Rechts der Isar, Technical University of Munich (TUM), Munich, Germany.
Leo NicolaiDepartment of Medicine I, University Hospital, Ludwig-Maximilians University Munich, Munich, Germany.
German Centre for Cardiovascular Research · DELudwig-Maximilians-Universität München · DETechnical University of Munich · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophils and platelets are among the most abundant cell types in peripheral blood and characterized by high plasticity and a readily available reservoir of surface proteins and secretable granule contents. Receptor-mediated activation and granule release predispose both cell types for rapid responses to various stimuli. While neutrophils provide the first line of defense to microbial infections and platelets are known for their aggregatory functions in hemostasis and thrombosis, research of the past decade has highlighted that both cell types jointly shape local and systemic immune responses and clot formation alike. Concomitant activation of neutrophils and platelets has been observed in a variety of cardiovascular diseases, including arterial and venous thrombosis, atherosclerosis as well as myocardial infarction and ischemia-reperfusion injury. In this review, we describe the mechanisms by which neutrophils and platelets interact physically, how release of granule contents and soluble molecules by either cell type affects the other and how this mutual activation supports the efficacy of immune responses. We go on to describe how activated platelets contribute to host defense by triggering neutrophil extracellular trap (NET) formation in a process termed immunothrombosis, which in turn promotes local platelet activation and coagulation. Further, we review current evidence of hazardous overactivation of either cell type and their respective role in cardiovascular disease, with a focus on thrombosis, myocardial infarction and ischemia-reperfusion injury, and describe how neutrophils and platelets shape thromboinflammation in COVID-19. Finally, we provide an overview of therapeutic approaches targeting neutrophil-platelet interactions as novel treatment strategy in cardiovascular disease.

Indexed as

cardiovascular diseaseNETosisneutrophilplateletthrombosis

Identifiers

PMID35174225
PMCPMC8841491
OpenAlexW4210537777

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.