Evidence map›Paper›PMID 27655025›Full record

ReviewInternal and emergency medicine2017

An exploratory look at NETosis in atherosclerosis.

Chiara Mozzini, Ulisse Garbin, Anna Maria Fratta Pasini, Luciano Cominacini

Abstract readReview
PubMed Publisher
In one paragraph

Review in Internal and emergency medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Review
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  7. Review
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  13. Review
  14. Review
  15. Inhibition of NETosis for treatment purposes: friend or foe?Molecular and cellular biochemistry · 2022
    Review
  16. Article
  17. Observational
  18. Article
  19. Article
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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 1 institution in 1 country.

Chiara MozziniSection of Internal Medicine, Department of Medicine, University of Verona, 10, Piazzale L.A. Scuro, 37134, Verona, Italy. chiaramozzini@libero.it.
Ulisse GarbinSection of Internal Medicine, Department of Medicine, University of Verona, 10, Piazzale L.A. Scuro, 37134, Verona, Italy.
Anna Maria Fratta PasiniSection of Internal Medicine, Department of Medicine, University of Verona, 10, Piazzale L.A. Scuro, 37134, Verona, Italy.
Luciano CominaciniSection of Internal Medicine, Department of Medicine, University of Verona, 10, Piazzale L.A. Scuro, 37134, Verona, Italy.
University of Verona · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Current evidence suggests the likelihood of a link between venous thromboembolism (VTE) and atherosclerosis, although they have been traditionally considered as different pathological entities. The contribution of neutrophils to human atherogenesis has been underestimated, if compared to their contribution established in VTE. This is due to the major importance attributed to macrophages in plaque destabilization. Nevertheless, the role of neutrophils in atherogenesis deserves increasing attention. In particular, neutrophil extracellular traps (NETs) are net-like chromatin fibres that are released from dying neutrophils. The death of neutrophils with NETs formation is called NETosis. During activation, neutrophils produce reactive oxygen species (ROS), through the activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. The main function of NETs is trapping and killing pathogens. Nevertheless, NETs formation has been observed in various chronic inflammatory diseases, autoimmune diseases, vasculitis, lung diseases, cancer and VTE. Recent studies suggest that NETs formation might contribute also to atherosclerosis progression. New data report the presence of NETs in the luminal portion of human atherosclerotic vessels and coronary specimens obtained from patients after acute myocardial infarction. Programmed death mechanisms in atherosclerosis such as apoptosis, efferocytosis and also NETosis, share common features and triggers. If defective, they can lead the cells to a switch from programmed death to necrosis, resulting in the release of pro-atherogenic factors, accumulation of cell debris and progression of the disease. This review provides evidence on the emerging role of neutrophils focusing on NETosis and oxidative stress burden in orchestrating common mechanisms in atherosclerosis and thrombosis.

Indexed as

Extracellular TrapsAtherosclerosisDiabetes MellitusHumansNeoplasmsNeutrophilsOxidative StressPulmonary Disease, Chronic ObstructiveVenous ThromboembolismAtherosclerosisCoronary artery diseaseNETosisOxidative stressVenous thromboembolism

Identifiers

PMID27655025
OpenAlexW2523355884

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.