Evidence map›Paper›PMID 32312382›Full record

ArticleeLife2020

Vascular permeability in retinopathy is regulated by VEGFR2 Y949 signaling to VE-cadherin.

Ross O Smith, Takeshi Ninchoji, Emma Gordon, Helder André, Elisabetta Dejana, Dietmar Vestweber, Anders Kvanta, Lena Claesson-Welsh

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 106 citations in OpenAlex.

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  15. Key Claudins at the Blood-Retina Barriers.Advances in experimental medicine and biology · 2025
    Review
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  17. Article
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  19. Article
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6 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

8 authors at 3 institutions in 2 countries.

Ross O SmithDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory Uppsala University, Uppsala, Sweden.ORCID 0000-0003-4239-3204
Takeshi NinchojiDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory Uppsala University, Uppsala, Sweden.
Emma GordonDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory Uppsala University, Uppsala, Sweden.
Helder AndréDepartment of Clinical Neuroscience, Division of Eye and Vision, St. Erik Eye Hospital, Karolinska Institutet, Stockholm, Sweden.
Elisabetta DejanaDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory Uppsala University, Uppsala, Sweden.
Dietmar VestweberMax Planck Institute for Molecular Biomedicine, Münster, Germany.ORCID 0000-0002-3517-732X
Anders KvantaDepartment of Clinical Neuroscience, Division of Eye and Vision, St. Erik Eye Hospital, Karolinska Institutet, Stockholm, Sweden.
Lena Claesson-WelshDepartment of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory Uppsala University, Uppsala, Sweden.ORCID 0000-0003-4275-2000
Uppsala University · SEKarolinska Institutet · SEMax Planck Institute for Molecular Biomedicine · DE

Funding

Australian Research Council DE170100167Fondation ARC pour la Recherche sur le Cancer AIRC IG 18683Fondation Leducq 17 CVD 03Knut och Alice Wallenbergs Stiftelse 2015.0030Knut och Alice Wallenbergs Stiftelse 2015.0275Vetenskapsrådet 2015-02375
6 · The paper itself

Abstract

Edema stemming from leaky blood vessels is common in eye diseases such as age-related macular degeneration and diabetic retinopathy. Whereas therapies targeting vascular endothelial growth factor A (VEGFA) can suppress leakage, side-effects include vascular rarefaction and geographic atrophy. By challenging mouse models representing different steps in VEGFA/VEGF receptor 2 (VEGFR2)-induced vascular permeability, we show that targeting signaling downstream of VEGFR2 pY949 limits vascular permeability in retinopathy induced by high oxygen or by laser-wounding. Although suppressed permeability is accompanied by reduced pathological neoangiogenesis in oxygen-induced retinopathy, similarly sized lesions leak less in mutant mice, separating regulation of permeability from angiogenesis. Strikingly, vascular endothelial (VE)-cadherin phosphorylation at the Y685, but not Y658, residue is reduced when VEGFR2 pY949 signaling is impaired. These findings support a mechanism whereby VE-cadherin Y685 phosphorylation is selectively associated with excessive vascular leakage. Therapeutically, targeting VEGFR2-regulated VE-cadherin phosphorylation could suppress edema while leaving other VEGFR2-dependent functions intact.

Indexed as

AnimalsCadherinsCapillary PermeabilityEndothelium, VascularMiceMice, Inbred C57BLRetinal DiseasesRetinal NeovascularizationSignal TransductionVascular Endothelial Growth Factor Receptor-2CadherinsKdr protein, mouseVascular Endothelial Growth Factor Receptor-2cell biologyhuman biologymacular edemamedicinemouseneovascularizationvascular endothelial growth factor receptorvascular permeability

Identifiers

PMID32312382
PMCPMC7188482
OpenAlexW3017094669

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.