Evidence map›Paper›PMID 42276988›Full record

ArticleCell death & disease2026

VEGFR2 deletion increases susceptibility to photoreceptor degeneration through glial-neuronal interaction.

Christina B Bielmeier, Sabrina I Schmitt, Verena Lehr, Anita Grundl, Andrea E Dillinger, Herbert Jägle, Christine von Toerne, Stefanie M Hauck, Süleyman Ergün, Ernst R Tamm and 3 more

Abstract read
In one paragraph

Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

13 authors.

Christina B Bielmeier *Institute of Neuroanatomy, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.
Sabrina I Schmitt *Institute of Human Anatomy and Embryology, University of Regensburg, Regensburg, Germany.
Verena LehrInstitute of Anatomy and Cell Biology, Julius-Maximilians-University, Wuerzburg, Germany.
Anita GrundlInstitute of Human Anatomy and Embryology, University of Regensburg, Regensburg, Germany.
Andrea E DillingerInstitute of Neuroanatomy, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.
Herbert JägleDepartment of Ophthalmology, University of Regensburg, Regensburg, Germany.
Christine von ToerneMetabolomics and Proteomics Core, Helmholtz Zentrum München, German Research Center for Environmental Health, Munich, Germany.ORCID http://orcid.org/0000-0002-4132-4322
Stefanie M HauckMetabolomics and Proteomics Core, Helmholtz Zentrum München, German Research Center for Environmental Health, Munich, Germany.
Süleyman ErgünInstitute of Neuroanatomy, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.ORCID http://orcid.org/0000-0002-2112-5377
Ernst R TammInstitute of Human Anatomy and Embryology, University of Regensburg, Regensburg, Germany.ORCID http://orcid.org/0000-0002-6679-8743
Anja SchlechtInstitute of Neuroanatomy, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.ORCID http://orcid.org/0000-0003-3336-9982
Andreas NeuederInstitute for Molecular Neurogenetics, Center for Molecular Neurobiology (ZMNH), University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany.
Barbara M BraungerInstitute of Neuroanatomy, University Medical Center Hamburg-Eppendorf (UKE), Hamburg, Germany. B.Braunger@uke.de.ORCID http://orcid.org/0000-0002-3926-6725

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) BR 4957/3-1
6 · The paper itself

Abstract

Intraocular anti-VEGFA injections are frequently used to counteract neovascularization in diseases such as the neovascular form of age-related macular degeneration (AMD). However, in the clinical context, patients with atrophic (dry) and neovascular (wet) AMD in the same eye will receive anti-VEGFA injections, but there are reports that this severely promotes the development of atrophic areas in dry AMD. To study this, we used mice with a tamoxifen-dependent deletion of Vegfr2 in the eye (Vegfr2

Indexed as

Gene DeletionMacular DegenerationNeurogliaNeuronsPhotoreceptor CellsPhotoreceptor Cells, VertebrateRetinal DegenerationVascular Endothelial Growth Factor Receptor-2AnimalsHumansMiceMice, Inbred C57BLMice, KnockoutSignal TransductionVascular Endothelial Growth Factor AKdr protein, mouseVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2

Identifiers

PMID42276988
PMCPMC13260824

What OpenQuestion holds

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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.