Evidence map›Paper›PMID 26912740›Full record

ArticleEMBO molecular medicine2016

Increased VEGF-A promotes multiple distinct aging diseases of the eye through shared pathomechanisms.

Alexander G Marneros

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Hypoxia-inducible factor-1 as targets for neuroprotection : from ferroptosis to Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

1 author at 1 institution in 1 country.

Alexander G MarnerosCutaneous Biology Research Center, Massachusetts General Hospital, Charlestown, MA, USA Department of Dermatology, Harvard Medical School, Boston, MA, USA amarneros@mgh.harvard.edu.
Massachusetts General Hospital · US

Funding

Molecular mechanisms of choroidal neovascularization and vascular homeostasisR01EY019297 · NEI · MASSACHUSETTS GENERAL HOSPITAL · PI MARNEROS, ALEXANDER GEORG · 2008 to 2011
$1.9M
NEI NIH HHS R01 EY019297NEI NIH HHS R01-EY019297
6 · The paper itself

Abstract

While increased VEGF-A has been associated with neovascular age-related macular degeneration (AMD), it is not known whether VEGF-A may also promote other age-related eye diseases. Here, we show that an increase in VEGF-A is sufficient to cause multiple distinct common aging diseases of the eye, including cataracts and both neovascular and non-exudative AMD-like pathologies. In the lens, increased VEGF-A induces age-related opacifications that are associated with ERK hyperactivation, increased oxidative damage, and higher expression of the NLRP3 inflammasome effector cytokine IL-1β. Similarly, increased VEGF-A induces oxidative stress and IL-1β expression also in the retinal pigment epithelium (RPE). Targeting NLRP3 inflammasome components or Il1r1 strongly inhibited not only VEGF-A-induced cataract formation, but also both neovascular and non-exudative AMD-like pathologies. Moreover, increased VEGF-A expression specifically in the RPE was sufficient to cause choroidal neovascularization (CNV) as in neovascular AMD, which could be inhibited by RPE-specific inactivation of Flk1, while Tlr2 inactivation strongly reduced CNV. These findings suggest a shared pathogenic role of VEGF-A-induced and NLRP3 inflammasome-mediated IL-1β activation for multiple distinct ocular aging diseases.

Indexed as

AgingAnimalsDisease Models, AnimalEye DiseasesInterleukin-1betaLens, CrystallineMiceNeovascularization, PathologicNLR Family, Pyrin Domain-Containing 3 ProteinRetinaVascular Endothelial Growth Factor AInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanVascular Endothelial Growth Factor Aage‐related macular degenerationagingcataractNLRP3 inflammasomeVEGF‐A

Identifiers

PMID26912740
PMCPMC4772957
OpenAlexW2278340732

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.