Evidence map›Paper›PMID 39097636›Full record

ArticleCommunications biology2024

Hydrostatic pressure drives sprouting angiogenesis via adherens junction remodelling and YAP signalling.

Dunja Alexandra Al-Nuaimi, Dominic Rütsche, Asra Abukar, Paul Hiebert, Dominik Zanetti, Nikola Cesarovic, Volkmar Falk, Sabine Werner, Edoardo Mazza, Costanza Giampietro

Abstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Review
  2. Article
  3. Vascular mechanical forces and vascular diseases.Journal of advanced research · 2026
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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.

Dunja Alexandra Al-NuaimiETH Zürich, DMAVT, Experimental Continuum Mechanics, Zürich, 8092, Switzerland.ORCID 0000-0002-5401-5326
Dominic RütscheEmpa, Swiss Federal Laboratories for Materials Science and Technology, Experimental Continuum Mechanics, Dübendorf, 8600, Switzerland.ORCID 0000-0001-6394-201X
Asra AbukarETH Zürich, DMAVT, Experimental Continuum Mechanics, Zürich, 8092, Switzerland.
Paul HiebertDepartment of Biology, ETH Zürich, Institute of Molecular Health Sciences, 8093, Zürich, Switzerland.
Dominik ZanettiDepartment of Biology, ETH Zürich, Institute of Molecular Health Sciences, 8093, Zürich, Switzerland.
Nikola CesarovicDepartment of Cardiothoracic and Vascular Surgery, German Heart Center Berlin, 13353, Berlin, Germany.
Volkmar FalkDepartment of Cardiothoracic and Vascular Surgery, German Heart Center Berlin, 13353, Berlin, Germany.
Sabine WernerDepartment of Biology, ETH Zürich, Institute of Molecular Health Sciences, 8093, Zürich, Switzerland.ORCID 0000-0001-7397-8710
Edoardo MazzaETH Zürich, DMAVT, Experimental Continuum Mechanics, Zürich, 8092, Switzerland. mazza@imes.mavt.ethz.ch.ORCID 0000-0001-9427-4157
Costanza GiampietroETH Zürich, DMAVT, Experimental Continuum Mechanics, Zürich, 8092, Switzerland. costanza.giampietro@empa.ch.ORCID 0000-0001-5229-3835

Funding

Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation) 205321_188828
6 · The paper itself

Abstract

Endothelial cell physiology is governed by its unique microenvironment at the interface between blood and tissue. A major contributor to the endothelial biophysical environment is blood hydrostatic pressure, which in mechanical terms applies isotropic compressive stress on the cells. While other mechanical factors, such as shear stress and circumferential stretch, have been extensively studied, little is known about the role of hydrostatic pressure in the regulation of endothelial cell behavior. Here we show that hydrostatic pressure triggers partial and transient endothelial-to-mesenchymal transition in endothelial monolayers of different vascular beds. Values mimicking microvascular pressure environments promote proliferative and migratory behavior and impair barrier properties that are characteristic of a mesenchymal transition, resulting in increased sprouting angiogenesis in 3D organotypic model systems ex vivo and in vitro. Mechanistically, this response is linked to differential cadherin expression at the adherens junctions, and to an increased YAP expression, nuclear localization, and transcriptional activity. Inhibition of YAP transcriptional activity prevents pressure-induced sprouting angiogenesis. Together, this work establishes hydrostatic pressure as a key modulator of endothelial homeostasis and as a crucial component of the endothelial mechanical niche.

Indexed as

Adherens JunctionsHydrostatic PressureNeovascularization, PhysiologicSignal TransductionYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingAnimalsCadherinsCell MovementEndothelial CellsHumansHuman Umbilical Vein Endothelial CellsTranscription FactorsAdaptor Proteins, Signal TransducingCadherinsTranscription FactorsYAP1 protein, humanYAP-Signaling Proteins

Identifiers

PMID39097636
PMCPMC11297954

What OpenQuestion holds

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LicenceCC BY
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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.