Evidence map›Paper›PMID 29234042›Full record

ArticleScientific reports2017

cfDNA correlates with endothelial damage after cardiac surgery with prolonged cardiopulmonary bypass and amplifies NETosis in an intracellular TLR9-independent manner.

Adnana Paunel-Görgülü, Max Wacker, Mouhamed El Aita, Shoreshfan Hassan, Georg Schlachtenberger, Antje Deppe, Yeong-Hoon Choi, Elmar Kuhn, Thorsten O Mehler, Thorsten Wahlers

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 2 pooled it
3.1field-weighted citation impact, top 7% 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

49 citing papers in PubMed, 2 syntheses or guidelines pooled it, 83 citations in OpenAlex.

  1. Pooled it
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  10. Fragmentation signatures in cancer patients resemble those of patients with vascular or autoimmune diseases.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  11. Article
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  14. Article
  15. Advances in cfDNA research for pregnancy-related diseases.Frontiers in cell and developmental biology · 2025
    Review
  16. %dd-cfDNA: The New Frontier for Heart/Lung Transplant Surveillance?Transplant international : official journal of the European Society for Organ Transplantation · 2025
    Review
  17. Review
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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

10 authors at 2 institutions in 1 country.

Adnana Paunel-GörgülüDepartment of Cardiothoracic Surgery, Heart Center of the University of Cologne, Cologne, Germany. adnana.paunel-goerguelue@uk-koeln.de.
Max WackerDepartment of Cardiothoracic Surgery, Heart Center of the University of Cologne, Cologne, Germany.
Mouhamed El AitaDepartment of Cardiothoracic Surgery, Heart Center of the University of Cologne, Cologne, Germany.
Shoreshfan HassanDepartment of Cardiothoracic Surgery, Heart Center of the University of Cologne, Cologne, Germany.
Georg SchlachtenbergerDepartment of Cardiothoracic Surgery, Heart Center of the University of Cologne, Cologne, Germany.
Antje DeppeDepartment of Cardiothoracic Surgery, Heart Center of the University of Cologne, Cologne, Germany.
Yeong-Hoon ChoiDepartment of Cardiothoracic Surgery, Heart Center of the University of Cologne, Cologne, Germany.
Elmar KuhnDepartment of Cardiothoracic Surgery, Heart Center of the University of Cologne, Cologne, Germany.
Thorsten O MehlerDepartment of Anaesthesiology and Intensive Care Medicine, University Hospital Cologne, Cologne, Germany.
Thorsten WahlersDepartment of Cardiothoracic Surgery, Heart Center of the University of Cologne, Cologne, Germany.
University Hospital Cologne · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiopulmonary bypass (CPB) provokes inflammation culminating in organ dysfunction and increased mortality. Recently, neutrophil extracellular traps (NETs) have been found to be involved in a variety of cardiovascular diseases promoting tissue and organ injury. Here, we aimed to elaborate the proinflammatory potential of circulating cell-free (cf)DNA in patients undergoing cardiac surgery with CPB. Plasma was collected pre- and postoperatively as well as at d1, d3, d5 and d8 after surgery. At d1, we found circulating cfDNA levels to be significantly increased in patients with prolonged CPB duration (>100 min) when compared to those with shorter CPB times (CPB < 100 min). Increased CPB duration yielded in higher levels of circulating mitochondrial (mt)DNA, soluble thrombomodulin (sCD141) and ICAM-1, reflecting endothelial damage. Positive correlation between cfDNA and sCD141 was demonstrated at all time points. Plasma and cfDNA from patients with CPB > 100 min induced NETs release by neutrophils from healthy donors which was not suppressed by inhibitors of intracellular toll-like receptor (TLR)9. DNA binding to neutrophils' surface (s)TLR9 has been evidenced. Altogether, we demonstrate that elevated plasma cfDNA might be useful to assess CPB-mediated detrimental effects, including endothelial damage, in cardiac surgical patients with prolonged CPB duration. cfDNA-triggered NETosis is independent of classical TLR9 signaling.

Indexed as

Cardiopulmonary BypassAdultAgedAntigens, SurfaceCell-Free Nucleic AcidsCells, CulturedDNA, MitochondrialExtracellular TrapsFemaleHumansIntracellular SpaceMaleMiddle AgedNeutrophilsOperative TimePilot ProjectsAntigens, SurfaceCell-Free Nucleic AcidsDNA, MitochondrialTHBD protein, humanThrombomodulinTLR9 protein, humanToll-Like Receptor 9

Identifiers

PMID29234042
PMCPMC5727170
OpenAlexW2775038098

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.