Evidence map›Paper›PMID 37822505›Full record

ArticleiScience2023

Endothelial barrier dysfunction in systemic inflammation is mediated by soluble VE-cadherin interfering VE-PTP signaling.

Juna-Lisa Knop, Natalie Burkard, Mahshid Danesh, Sebastian Kintrup, Thomas Dandekar, Mugdha Srivastava, Rebecca Springer, Matthias Hiermaier, Nana-Maria Wagner, Jens Waschke and 2 more

Abstract read
In one paragraph

Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. ZEB1 Modifies VE-Cadherin Signaling in Lymphatic Endothelial Cells.Microcirculation (New York, N.Y. : 1994) · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Roles of endothelial cells during infection.Current opinion in immunology · 2025
    Review
  6. Review
  7. Article
  8. Article
  9. 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

12 authors.

Juna-Lisa KnopDepartment of General, Visceral, Transplantation, Vascular and Paediatric Surgery (Department of Surgery I), University Hospital Wuerzburg, Oberduerrbacherstraße 6, D-97080 Wuerzburg, Germany.
Natalie BurkardDepartment of General, Visceral, Transplantation, Vascular and Paediatric Surgery (Department of Surgery I), University Hospital Wuerzburg, Oberduerrbacherstraße 6, D-97080 Wuerzburg, Germany.
Mahshid DaneshUniversity of Wuerzburg, Department of Bioinformatics, Biocenter, Am Hubland, D-97074 Wuerzburg, Germany.
Sebastian KintrupUniversity Hospital Muenster, Department of Anesthesiology, Intensive Care and Pain Medicine, Albert-Schweitzer-Campus 1, 48149 Muenster, Germany.
Thomas DandekarUniversity of Wuerzburg, Department of Bioinformatics, Biocenter, Am Hubland, D-97074 Wuerzburg, Germany.
Mugdha SrivastavaCore Unit Systems Medicine, 97080 Würzburg, Germany.
Rebecca SpringerDepartment of General, Visceral, Transplantation, Vascular and Paediatric Surgery (Department of Surgery I), University Hospital Wuerzburg, Oberduerrbacherstraße 6, D-97080 Wuerzburg, Germany.
Matthias HiermaierChair of Vegetative Anatomy, Institute of Anatomy, Faculty of Medicine, LMU Munich, Munich, Germany.
Nana-Maria WagnerUniversity Hospital Muenster, Department of Anesthesiology, Intensive Care and Pain Medicine, Albert-Schweitzer-Campus 1, 48149 Muenster, Germany.
Jens WaschkeChair of Vegetative Anatomy, Institute of Anatomy, Faculty of Medicine, LMU Munich, Munich, Germany.
Sven FlemmingDepartment of General, Visceral, Transplantation, Vascular and Paediatric Surgery (Department of Surgery I), University Hospital Wuerzburg, Oberduerrbacherstraße 6, D-97080 Wuerzburg, Germany.
Nicolas SchlegelDepartment of General, Visceral, Transplantation, Vascular and Paediatric Surgery (Department of Surgery I), University Hospital Wuerzburg, Oberduerrbacherstraße 6, D-97080 Wuerzburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breakdown of endothelial barrier integrity determines organ dysfunction and outcome of patients with sepsis. Increased levels of soluble vascular endothelial (VE)-cadherin fragments (sVE-cadherin) have previously been linked with inflammation-induced loss of endothelial barrier function. We provide evidence for a causative role of sVE-cadherin to induce loss of endothelial barrier function. In patients with sepsis, sVE-cadherin levels were associated with organ dysfunction and the need for volume resuscitation. Similarly, LPS-induced systemic inflammation in rats with microvascular dysfunction was paralleled by augmented sVE-cadherin levels. Newly generated recombinant human sVE-cadherin (extracellular domains EC1-5) induced loss of endothelial barrier function in both human microvascular endothelial cells

Indexed as

Biological sciencesCell biologyMolecular biology

Identifiers

PMID37822505
PMCPMC10563049

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.