ArticleeLife2021
eNOS-induced vascular barrier disruption in retinopathy by c-Src activation and tyrosine phosphorylation of VE-cadherin.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- Association of endothelial nitric oxide synthase (NOS3) rs2070744 variant with advanced retinopathy of prematurity: a case-control study and meta-analysis.Scientific reports · 2025Pooled it
- VEGFAngiogenesis · 2026Article
- Putative mechanisms of ocular inflammation in syphilis.Journal of ophthalmic inflammation and infection · 2026Review
- Disrupting VE-cadherin Y685 phosphorylation inhibits development of experimental diabetic and prediabetic retinopathy.The Journal of clinical investigation · 2026Article
- Exosomal miR-92a-3p promotes pancreatic cancer cells' extravasation by inducing vascular permeability through inhibition of DAB2IP.Cell death & disease · 2026Article
- SHP2 regulates VEGFR2 Y1175/PLCγ signaling to impair tumor endothelial barrier stability.iScience · 2026Article
- Pulmonary hypertension, inhaled nitric oxide, and retinopathy of prematurity: evidence from the U.S. national database.Pediatric research · 2026Article
- Protective Effects of Luteolin onAntibiotics (Basel, Switzerland) · 2025Article
- Bidirectional Phosphorylation Changes in Opsins Associated With Early Myopia and Hyperopia Signal Regulation by Phosphoproteomics.Investigative ophthalmology & visual science · 2025Article
- Zinc sulfate gel reshapes the wound microenvironment to promote full-thickness wound healing in mice.Regenerative therapy · 2025Article
- Citrulline Plus Arginine Induces an Angiogenic Response and Increases Permeability in Retinal Endothelial Cells via Nitric Oxide Production.International journal of molecular sciences · 2025Article
- Beyond monoclonal antibodies: constraints and the case for alternative PD-1/PD-L1-targeting formats.Frontiers in immunology · 2025Review
- Article
- Systemic capillary leak syndrome.Nature reviews. Disease primers · 2024Review
- A New Ex Vivo Model Based on Mouse Retinal Explants for the Study of Ocular Toxoplasmosis.Pathogens (Basel, Switzerland) · 2024Article
- Article
- c-Src-induced vascular malformations require localised matrix degradation at focal adhesions.Journal of cell science · 2024Article
- Unraveling Endothelial Cell Migration: Insights into Fundamental Forces, Inflammation, Biomaterial Applications, and Tissue Regeneration Strategies.ACS applied bio materials · 2024Review
- Intrinsic endothelial hyperresponsiveness to inflammatory mediators drives acute episodes in models of Clarkson disease.The Journal of clinical investigation · 2024Article
- The BulkECexplorer compiles endothelial bulk transcriptomes to predict functional versus leaky transcription.Nature cardiovascular research · 2024Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Background: Hypoxia and consequent production of vascular endothelial growth factor A (VEGFA) promote blood vessel leakiness and edema in ocular diseases. Anti-VEGFA therapeutics may aggravate hypoxia; therefore, therapy development is needed. Methods: Oxygen-induced retinopathy was used as a model to test the role of nitric oxide (NO) in pathological neovascularization and vessel permeability. Suppression of NO formation was achieved chemically using L-NMMA, or genetically, in endothelial NO synthase serine to alanine (S1176A) mutant mice. Results: Suppression of NO formation resulted in reduced retinal neoangiogenesis. Remaining vascular tufts exhibited reduced vascular leakage through stabilized endothelial adherens junctions, manifested as reduced phosphorylation of vascular endothelial (VE)-cadherin Y685 in a c-Src-dependent manner. Treatment with a single dose of L-NMMA in established retinopathy restored the vascular barrier and prevented leakage. Conclusions: We conclude that NO destabilizes adheren junctions, resulting in vascular hyperpermeability, by converging with the VEGFA/VEGFR2/c-Src/VE-cadherin pathway. Funding: This study was supported by the Swedish Cancer foundation (19 0119 Pj ), the Swedish Research Council (2020-01349), the Knut and Alice Wallenberg foundation (KAW 2020.0057) and a Fondation Leducq Transatlantic Network of Excellence Grant in Neurovascular Disease (17 CVD 03). KAW also supported LCW with a Wallenberg Scholar grant (2015.0275). WCS was supported by Grants R35 HL139945, P01 HL1070205, AHA MERIT Award. DV was supported by grants from the Deutsche Forschungsgemeinschaft, SFB1450, B03, and CRU342, P2.
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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.