Evidence map›Paper›PMID 32710087›Full record

ArticleScientific reports2020

VEGF is an autocrine/paracrine neuroprotective factor for injured retinal ganglion neurons.

Nicolas Froger, Frédéric Matonti, Christophe Roubeix, Valérie Forster, Ivana Ivkovic, Nadège Brunel, Christophe Baudouin, José-Alain Sahel, Serge Picaud

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
8.1field-weighted citation impact, top 2% 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, 80 citations in OpenAlex.

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  10. Anti-VEGF Agents Clearance Through the Aqueous Outflow Pathway in a Rat Model.Investigative ophthalmology & visual science · 2025
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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

9 authors at 2 institutions in 2 countries.

Nicolas FrogerSorbonne Université, INSERM, CNRS, Institut de La Vision, 17 rue Moreau, 75012, Paris, France. nifroger@yahoo.fr.
Frédéric MatontiSorbonne Université, INSERM, CNRS, Institut de La Vision, 17 rue Moreau, 75012, Paris, France.
Christophe RoubeixSorbonne Université, INSERM, CNRS, Institut de La Vision, 17 rue Moreau, 75012, Paris, France.
Valérie ForsterSorbonne Université, INSERM, CNRS, Institut de La Vision, 17 rue Moreau, 75012, Paris, France.
Ivana IvkovicSorbonne Université, INSERM, CNRS, Institut de La Vision, 17 rue Moreau, 75012, Paris, France.
Nadège BrunelUMS 29 INSERM Plateforme FluExGen UPMC, 75012, Paris, France.
Christophe BaudouinSorbonne Université, INSERM, CNRS, Institut de La Vision, 17 rue Moreau, 75012, Paris, France.
José-Alain SahelSorbonne Université, INSERM, CNRS, Institut de La Vision, 17 rue Moreau, 75012, Paris, France.
Serge PicaudSorbonne Université, INSERM, CNRS, Institut de La Vision, 17 rue Moreau, 75012, Paris, France. serge.picaud@inserm.fr.ORCID https://orcid.org/0000-0002-0548-5145
Centre National de la Recherche Scientifique · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular endothelial growth factor-A (VEGF) is the angiogenic factor promoting the pathological neovascularization in age-related macular degeneration (AMD) or diabetic macular edema (DME). Evidences have suggested a neurotrophic and neuroprotective role of VEGF, albeit in retina, cellular mechanisms underlying the VEGF neuroprotection remain elusive. Using purified adult retinal ganglion cells (RGCs) in culture, we demonstrated here that VEGF is released by RGCs themselves to promote their own survival, while VEGF neutralization by specific antibodies or traps drastically reduced the RGC survival. These results indicate an autocrine VEGF neuroprotection on RGCs. In parallel, VEGF produced by mixed retinal cells or by mesenchymal stem cells exerted a paracrine neuroprotection on RGCs. Such neuroprotective effect was obtained using the recombinant VEGF-B, suggesting the involvement of VEGF-R1 pathway in VEGF-elicited RGC survival. Finally, glaucomatous patients injected with VEGF traps (ranibizumab or aflibercept) due to either AMD or DME comorbidity, showed a significant reduction of RGC axon fiber layer thickness, consistent with the plausible reduction of the VEGF autocrine stimulation of RGCs. Our results provide evidence of the autocrine neuroprotective function of VEGF on RGCs is crucially involved to preserve injured RGCs such as in glaucomatous patients.

Indexed as

AgedAged, 80 and overAnimalsAutocrine CommunicationCells, CulturedCell SurvivalDiabetic RetinopathyFemaleGlaucomaHumansIntravitreal InjectionsMacular DegenerationMacular EdemaMaleMesenchymal Stem CellsMiddle AgedafliberceptFLT1 protein, humanRanibizumabReceptors, Vascular Endothelial Growth FactorRecombinant Fusion ProteinsRecombinant ProteinsVascular Endothelial Growth Factor Avascular endothelial growth factor A, ratVascular Endothelial Growth Factor BVascular Endothelial Growth Factor Receptor-1VEGFA protein, humanVEGFB protein, human

Identifiers

PMID32710087
PMCPMC7382485
OpenAlexW3044951523

What OpenQuestion holds

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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.