ArticleInvestigative ophthalmology & visual science2017
VEGF as a Paracrine Regulator of Conventional Outflow Facility.
Article in Investigative ophthalmology & visual science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 39 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Advances in glaucoma biomechanics from 2000 to 2024: a bibliometric study and visualization analysis.Frontiers in neuroscience · 2025Pooled it
- VEGFA-Positive Macrophages Regulate Aqueous Humor Outflow in Aged Mice and Humans.bioRxiv : the preprint server for biology · 2026Article
- Transcriptomic Profiling of High vs. Low Flow Regions of Mouse and Human Trabecular Meshwork.bioRxiv : the preprint server for biology · 2026Article
- Assessment of anti-VEGF intravitreal injection effects on murine neonatal Schlemm's canal morphology.Scientific reports · 2026Article
- Article
- Effects of ascorbic acid on trabecular meshwork gene expression and collagen secretion.BMJ open ophthalmology · 2026Article
- Article
- Single-cell profiling of trabecular meshwork identifies mitochondrial dysfunction in a glaucoma model that is protected by vitamin B3 treatment.bioRxiv : the preprint server for biology · 2025Article
- Anti-VEGF Agents Clearance Through the Aqueous Outflow Pathway in a Rat Model.Investigative ophthalmology & visual science · 2025Article
- Fibrosis and Src Signalling in Glaucoma: From Molecular Pathways to Therapeutic Prospects.International journal of molecular sciences · 2025Review
- FYN regulates aqueous humor outflow and IOP through the phosphorylation of VE-CADHERIN.Nature communications · 2025Article
- The role of YAP/TAZ mechanosignaling in trabecular meshwork and Schlemm's canal cell dysfunction.Vision research · 2024Review
- Article
- Transcriptomic profiling of Schlemm's canal cells reveals a lymphatic-biased identity and three major cell states.bioRxiv : the preprint server for biology · 2024Article
- Profiling IOP-Responsive Genes in the Trabecular Meshwork and Optic Nerve Head in a Rat Model of Controlled Elevation of Intraocular Pressure.Investigative ophthalmology & visual science · 2024Article
- VEGF-A-induced changes in distal outflow tract structure and function.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2024Article
- The Association of Primary Open Angle Glaucoma and Ocular Hypertension with Anti-VEGF Injections.Clinical ophthalmology (Auckland, N.Z.) · 2024Article
- Long-term surveillance provides real-world evidences of safety and effectiveness in intravitreal aflibercept treatment for age-related macular degeneration.Scientific reports · 2023Observational
- High VEGF Concentrations Accelerate Human Trabecular Meshwork Fibrosis in a TAZ-Dependent Manner.International journal of molecular sciences · 2023Article
- Measurement of postmortem outflow facility using iPerfusion.Experimental eye research · 2022Article
Corrections and comments
- Erratum issuedErratum.2017
Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
Purpose: Vascular endothelial growth factor (VEGF) regulates microvascular endothelial permeability, and the permeability of Schlemm's canal (SC) endothelium influences conventional aqueous humor outflow. We hypothesize that VEGF signaling regulates outflow facility. Methods: We measured outflow facility (C) in enucleated mouse eyes perfused with VEGF-A164a, VEGF-A165b, VEGF-D, or inhibitors to VEGF receptor 2 (VEGFR-2). We monitored VEGF-A secretion from human trabecular meshwork (TM) cells by ELISA after 24 hours of static culture or cyclic stretch. We used immunofluorescence microscopy to localize VEGF-A protein within the TM of mice. Results: VEGF-A164a increased C in enucleated mouse eyes. Cyclic stretch increased VEGF-A secretion by human TM cells, which corresponded to VEGF-A localization in the TM of mice. Blockade of VEGFR-2 decreased C, using either of the inhibitors SU5416 or Ki8751 or the inactive splice variant VEGF-A165b. VEGF-D increased C, which could be blocked by Ki8751. Conclusions: VEGF is a paracrine regulator of conventional outflow facility that is secreted by TM cells in response to mechanical stress. VEGF affects facility via VEGFR-2 likely at the level of SC endothelium. Disruption of VEGF signaling in the TM may explain why anti-VEGF therapy is associated with decreased outflow facility and sustained ocular hypertension.
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Registered trials
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.