Evidence map›Paper›PMID 37053273›Full record

ReviewCirculation research2023

NETs-Induced Thrombosis Impacts on Cardiovascular and Chronic Kidney Disease.

Manovriti Thakur, Carolina Victoria Cruz Junho, Sarah Maike Bernhard, Marc Schindewolf, Heidi Noels, Yvonne Döring

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Circulation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
13.0field-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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

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  20. mFrontiers in immunology · 2026
    Review

4 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

6 authors at 3 institutions in 3 countries.

Manovriti ThakurDivision of Angiology, Swiss Cardiovascular Center, Inselspital (M.T., S.M.B., M.S., Y.D.), Bern University Hospital, University of Bern, Switzerland.ORCID 0000-0003-3825-4121
Carolina Victoria Cruz JunhoInstitute for Molecular Cardiovascular Research (IMCAR), University Hospital RWTH Aachen, Germany (C.V.C.J., H.N.).
Sarah Maike BernhardDivision of Angiology, Swiss Cardiovascular Center, Inselspital (M.T., S.M.B., M.S., Y.D.), Bern University Hospital, University of Bern, Switzerland.
Marc SchindewolfDivision of Angiology, Swiss Cardiovascular Center, Inselspital (M.T., S.M.B., M.S., Y.D.), Bern University Hospital, University of Bern, Switzerland.
Heidi NoelsInstitute for Molecular Cardiovascular Research (IMCAR), University Hospital RWTH Aachen, Germany (C.V.C.J., H.N.).ORCID 0000-0003-3053-6984
Yvonne DöringDivision of Angiology, Swiss Cardiovascular Center, Inselspital (M.T., S.M.B., M.S., Y.D.), Bern University Hospital, University of Bern, Switzerland.ORCID 0000-0001-9307-3396
University of Bern · CHMaastricht University · NLRWTH Aachen University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arterial and venous thrombosis constitute a major source of morbidity and mortality worldwide. Association between thrombotic complications and cardiovascular and other chronic inflammatory diseases are well described. Inflammation and subsequent initiation of thrombotic events, termed immunothrombosis, also receive growing attention but are still incompletely understood. Nevertheless, the clinical relevance of aberrant immunothrombosis, referred to as thromboinflammation, is evident by an increased risk of thrombosis and cardiovascular events in patients with inflammatory or infectious diseases. Proinflammatory mediators released from platelets, complement activation, and the formation of NETs (neutrophil extracellular traps) initiate and foster immunothrombosis. In this review, we highlight and discuss prominent and emerging interrelationships and functions between NETs and other mediators in immunothrombosis in cardiovascular disease. Also, with patients with chronic kidney disease suffering from increased cardiovascular and thrombotic risk, we summarize current knowledge on neutrophil phenotype, function, and NET formation in chronic kidney disease. In addition, we elaborate on therapeutic targeting of NETs-induced immunothrombosis. A better understanding of the functional relevance of antithrombotic mediators which do not increase bleeding risk may provide opportunities for successful therapeutic interventions to reduce thrombotic risk beyond current treatment options.

Indexed as

Extracellular TrapsRenal Insufficiency, ChronicThrombosisHumansInflammationNeutrophilsThromboinflammationcardiovascular diseasesinflammationkidneyneutrophilsthrombosis

Identifiers

PMID37053273
PMCPMC10377271
OpenAlexW4365460191

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.