Evidence map›Paper›PMID 26113211›Full record

ReviewProgress in retinal and eye research2015

Molecular pathogenesis of retinal and choroidal vascular diseases.

Peter A Campochiaro

Open access · greenAbstract readReview
In one paragraph

Review in Progress in retinal and eye research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 318 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
318citing papers in PubMed, 3 pooled it
33.0field-weighted citation impact, top 1% 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

318 citing papers in PubMed, 3 syntheses or guidelines pooled it, 520 citations in OpenAlex.

  1. Pooled it
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  3. Pooled it
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  6. Review
  7. Article
  8. Review
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  10. Article
  11. Case series: The role of retinal ischemia in the pathogenesis and clinical manifestation of diabetic retinopathy.Optometry and vision science : official publication of the American Academy of Optometry · 2026
    Article
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  13. Review
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  20. A real-world study of Faricimab: efficacy and biomarkers in treatment-experienced neovascular age-related macular degeneration(nAMD) and diabetic macular edema (DME) patients.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026
    Article

258 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

1 author at 1 institution in 1 country.

Peter A CampochiaroDepartments of Ophthalmology and Neuroscience, Maumenee 815, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Baltimore, MD 21287-9277, USA. Electronic address: pcampo@jhmi.edu.
Johns Hopkins Medicine · US

Funding

Targeting survival factors for ocular neovascularizationR01EY012609 · NEI · JOHNS HOPKINS UNIVERSITY · PI CAMPOCHIARO, PETER A · 1999 to 2015
$5.3M
NEI NIH HHS EY012609NEI NIH HHS R01 EY012609
6 · The paper itself

Abstract

There are two major types of ocular neovascularization that affect the retina, retinal neovascularization (NV) and subretinal or choroidal NV. Retinal NV occurs in a group of diseases referred to as ischemic retinopathies in which damage to retinal vessels results in retinal ischemia. Most prevalent of these are diabetic retinopathy and retinal vein occlusions. Subretinal and choroidal NV occur in diseases of the outer retina and Bruch's membrane, the most prevalent of which is age-related macular degeneration. Numerous studies in mouse models have helped to elucidate the molecular pathogenesis underlying retinal, subretinal, and choroidal NV. There is considerable overlap because the precipitating event in each is stabilization of hypoxia inducible factor-1 (HIF-1) which leads to upregulation of several hypoxia-regulated gene products, including vascular endothelial growth factor (VEGF), angiopoietin 2, vascular endothelial-protein tyrosine phosphatase (VE-PTP), and several others. Stimulation of VEGF signaling and suppression of Tie2 by angiopoietin 2 and VE-PTP are critical for sprouting of retinal, subretinal, and choroidal NV, with perturbation of Bruch's membrane also needed for the latter. Additional HIF-1-regulated gene products cause further stimulation of the NV. It is difficult to model macular edema in animals and therefore proof-of-concept clinical trials were done and demonstrated that VEGF plays a central role and that suppression of Tie2 is also important. Neutralization of VEGF is currently the first line therapy for all of the above disease processes, but new treatments directed at some of the other molecular targets, particularly stabilization of Tie2, are likely to provide additional benefit for subretinal/choroidal NV and macular edema. In addition, the chronicity of these diseases as well as the implication of VEGF as a cause of retinal nonperfusion and progression of background diabetic retinopathy make sustained delivery approaches for VEGF antagonists a priority.

Indexed as

Angiogenesis InhibitorsAngiopoietin-2AnimalsChoroid DiseasesDisease Models, AnimalHumansHypoxia-Inducible Factor 1Intercellular Signaling Peptides and ProteinsMiceNeovascularization, PathologicRetinal DiseasesVascular Endothelial Growth Factor AAngiogenesis InhibitorsAngiopoietin-2Hypoxia-Inducible Factor 1Intercellular Signaling Peptides and ProteinsVascular Endothelial Growth Factor AAge-related macular degenerationAngiogenesisAngiopoietinsDiabetic retinopathyHypoxia-inducible factor-1Platelet-derived growth factorTIE2Vascular endothelial growth factorVascular endothelial-protein tyrosine phosphatase

Identifiers

PMID26113211
PMCPMC4651818
OpenAlexW763617670

What OpenQuestion holds

Textmetadata
LicenceTDM
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.