Evidence map›Paper›PMID 32917003›Full record

ArticleCells2020

Fibrotic Changes and Endothelial-to-Mesenchymal Transition Promoted by VEGFR2 Antagonism Alter the Therapeutic Effects of VEGFA Pathway Blockage in a Mouse Model of Choroidal Neovascularization.

Franco Aparecido Rossato, Yu Su, Ashley Mackey, Yin Shan Eric Ng

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

22 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Management of fibrosis in neovascular age-related macular degeneration.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026
    Review
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  6. Review
  7. Article
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  11. Angiopoietin-2 associates with poor prognosis in Moyamoya angiopathy.Annals of clinical and translational neurology · 2024
    Article
  12. Article
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  15. Review
  16. Article
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  19. Comparison of before versus after intravitreal bevacizumab injection, growth factor levels and fibrotic markers in vitreous samples from patients with proliferative diabetic retinopathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022
    Article
  20. 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

4 authors at 1 institution in 2 countries.

Franco Aparecido RossatoDepartment of Ophthalmology, Schepens Eye Research Institute of Mass Eye and Ear, and Harvard Medical School, 20 Staniford Street, Boston, MA 02114, USA.
Yu SuDepartment of Ophthalmology, Schepens Eye Research Institute of Mass Eye and Ear, and Harvard Medical School, 20 Staniford Street, Boston, MA 02114, USA.
Ashley MackeyDepartment of Ophthalmology, Schepens Eye Research Institute of Mass Eye and Ear, and Harvard Medical School, 20 Staniford Street, Boston, MA 02114, USA.
Yin Shan Eric NgDepartment of Ophthalmology, Schepens Eye Research Institute of Mass Eye and Ear, and Harvard Medical School, 20 Staniford Street, Boston, MA 02114, USA.ORCID 0000-0002-4982-1999
Massachusetts Eye and Ear Infirmary · US

Funding

VISION RESEARCHP30EY003790 · NEI · SCHEPENS EYE RESEARCH INSTITUTE · PI Patricia Ann D'Amore · 1985 to 2026
$25.5M
NEI NIH HHS P30 EY003790
6 · The paper itself

Abstract

Many patients with wet age-related macular degeneration do not respond well to anti- vascular endothelial growth factor A (VEGFA) therapy for choroidal neovascularization (CNV), and the efficacy of anti-VEGFA decreases over time. We investigated the hypothesis that fibrotic changes, in particular via endothelial-to-mesenchymal transition (EndoMT), play a role in CNV and alter the therapeutic effects of VEGFA pathway blockage. Induction of EndoMT of primary human retinal endothelial cells led to a significantly reduced response to VEGFA at the level of gene expression, cellular proliferation, migration, and tube formation. Suppression of EndoMT restored cell responsiveness to VEGFA. In a mouse model of spontaneous CNV, fibrotic changes and EndoMT persisted as the CNV lesions became more established over time. VEGFA receptor-2 (VEGFR2) antagonism further induced fibrosis and EndoMT in the CNV. The combination of VEGFR2 antagonism and fibrosis/EndoMT inhibition was more effective than either individual treatment in reducing CNV. Our data indicate that fibrosis and EndoMT are involved in the progression of CNV, are exacerbated by VEGFR2 inhibition, and could provide an explanation for the reduced efficacy of anti-VEGFA treatment over time.

Indexed as

AnimalsChoroidal NeovascularizationDisease Models, AnimalEndothelial CellsHumansMiceVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Aage-related macular degenerationchoroidal neovascularizationendothelial-to-mesenchymal transitionVEGFAVEGFA resistance

Identifiers

PMID32917003
PMCPMC7563259
OpenAlexW3084055592

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.