Evidence map›Paper›PMID 28530658›Full record

ArticleNature cell biology2017

Endoglin controls blood vessel diameter through endothelial cell shape changes in response to haemodynamic cues.

Wade W Sugden, Robert Meissner, Tinri Aegerter-Wilmsen, Roman Tsaryk, Elvin V Leonard, Jeroen Bussmann, Mailin J Hamm, Wiebke Herzog, Yi Jin, Lars Jakobsson and 2 more

Open access · greenAbstract readVideo-Audio Media
In one paragraph

Article in Nature cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
9.9field-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

117 citing papers in PubMed, 214 citations in OpenAlex.

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  9. Swimming motions evoke Piezo1-dependent CaCurrent biology : CB · 2025
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57 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 5 institutions in 3 countries.

Wade W SugdenMax Planck Institute for Molecular Biomedicine, Roentgenstrasse 20, D-48149 Muenster, Germany.
Robert MeissnerCells-in-Motion Cluster of Excellence (EXC 1003 - CiM), University of Muenster, D-48149 Muenster, Germany.
Tinri Aegerter-WilmsenInstitute of Molecular Life Sciences, University of Zurich, Winterthurerstrasse 190, 8057 Zurich, Switzerland.
Roman TsarykMax Planck Institute for Molecular Biomedicine, Roentgenstrasse 20, D-48149 Muenster, Germany.
Elvin V LeonardMax Planck Institute for Molecular Biomedicine, Roentgenstrasse 20, D-48149 Muenster, Germany.
Jeroen BussmannMax Planck Institute for Molecular Biomedicine, Roentgenstrasse 20, D-48149 Muenster, Germany.
Mailin J HammMax Planck Institute for Molecular Biomedicine, Roentgenstrasse 20, D-48149 Muenster, Germany.
Wiebke HerzogMax Planck Institute for Molecular Biomedicine, Roentgenstrasse 20, D-48149 Muenster, Germany.
Yi JinKarolinska Institute, Department of Medical Biochemistry and Biophysics, SE 171 77 Stockholm, Sweden.
Lars JakobssonKarolinska Institute, Department of Medical Biochemistry and Biophysics, SE 171 77 Stockholm, Sweden.ORCID http://orcid.org/0000-0001-7956-587X
Cornelia DenzCells-in-Motion Cluster of Excellence (EXC 1003 - CiM), University of Muenster, D-48149 Muenster, Germany.
Arndt F SiekmannMax Planck Institute for Molecular Biomedicine, Roentgenstrasse 20, D-48149 Muenster, Germany.ORCID http://orcid.org/0000-0001-6972-2173
Augenstern · DEUniversity of Münster · DEKarolinska Institutet · SEMax Planck Institute for Molecular Biomedicine · DEUniversity of Zurich · CH

Funding

European Research Council 260794
6 · The paper itself

Abstract

The hierarchical organization of properly sized blood vessels ensures the correct distribution of blood to all organs of the body, and is controlled via haemodynamic cues. In current concepts, an endothelium-dependent shear stress set point causes blood vessel enlargement in response to higher flow rates, while lower flow would lead to blood vessel narrowing, thereby establishing homeostasis. We show that during zebrafish embryonic development increases in flow, after an initial expansion of blood vessel diameters, eventually lead to vessel contraction. This is mediated via endothelial cell shape changes. We identify the transforming growth factor beta co-receptor endoglin as an important player in this process. Endoglin mutant cells and blood vessels continue to enlarge in response to flow increases, thus exacerbating pre-existing embryonic arterial-venous shunts. Together, our data suggest that cell shape changes in response to biophysical cues act as an underlying principle allowing for the ordered patterning of tubular organs.

Indexed as

Cell ShapeHemodynamicsMechanotransduction, CellularAnimalsArteriovenous MalformationsEndoglinEndothelial CellsGenetic Predisposition to DiseaseHumansHuman Umbilical Vein Endothelial CellsKruppel-Like Transcription FactorsMice, KnockoutMutationNeovascularization, PhysiologicPhenotypeRegional Blood FlowEndoglinEng protein, mouseEng protein, zebrafishKlf2a protein, zebrafishKruppel-Like Transcription FactorsZebrafish Proteins

Identifiers

PMID28530658
PMCPMC5455977
OpenAlexW2619222934

What OpenQuestion holds

Textmetadata
LicenceTDM
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.