ArticleThe American journal of pathology2015
Novel CCR3 Antagonists Are Effective Mono- and Combination Inhibitors of Choroidal Neovascular Growth and Vascular Permeability.
Article in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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Who cites it
23 citing papers in PubMed, 27 citations in OpenAlex.
- Safety and Efficacy of cceAAV-aflibercept-Fc-YTE (F-CRG-B191): A Gene Therapy for Neovascular Age-Related Macular Degeneration.Investigative ophthalmology & visual science · 2026Article
- Diosgenin mitigates laser-induced choroidal neovascularization by suppressing the endothelial-to-mesenchymal transition via the TGF-β/Smad and MAPKs signaling pathways.American journal of translational research · 2026Article
- Circulating Inflammatory Proteins and Age-related Macular Degeneration: New Insights from Mendelian Randomization.Combinatorial chemistry & high throughput screening · 2026Article
- JR5558 mice are a reliable model to investigate subretinal fibrosis.Scientific reports · 2024Article
- CCR3 Expression in Relation to Delayed Microbleeds in a Rat Model of Large Vessel Occlusion.Journal of experimental neurology · 2024Article
- Review
- Choroidal neovascularization removal with photo-mediated ultrasound therapy.Medical physics · 2023Article
- Clinical Pathological Features and Current Animal Models of Type 3 Macular Neovascularization.Frontiers in neuroscience · 2021Review
- Article
- Article
- Chronic Dicer1 deficiency promotes atrophic and neovascular outer retinal pathologies in mice.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Targeting the Notch and TGF-β signaling pathways to prevent retinal fibrosisTheranostics · 2020Article
- Secretogranin III as a novel target for the therapy of choroidal neovascularization.Experimental eye research · 2019Article
- Spontaneous Posterior Segment Vascular Disease Phenotype of a Mouse Model, rnv3, Is Dependent on the Crb1rd8 Allele.Investigative ophthalmology & visual science · 2018Article
- Retinal Vasculature in Development and Diseases.Annual review of vision science · 2018Review
- [Chemokines in ophthalmology].Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft · 2018Review
- Secretogranin III: a diabetic retinopathy-selective angiogenic factor.Cellular and molecular life sciences : CMLS · 2018Review
- Animal models of ocular angiogenesis: from development to pathologies.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Review
- Expression of CCR3, SOX5 and LC3 in patients with elderly onset rheumatoid arthritis and the clinical significance.Experimental and therapeutic medicine · 2017Article
- A Proinflammatory Function of Toll-Like Receptor 2 in the Retinal Pigment Epithelium as a Novel Target for Reducing Choroidal Neovascularization in Age-Related Macular Degeneration.The American journal of pathology · 2017Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Choroidal neovascularization (CNV) is a defining feature of wet age-related macular degeneration. We examined the functional role of CCR3 in the development of CNV in mice and primates. CCR3 was associated with spontaneous CNV lesions in the newly described JR5558 mice, whereas CCR3 ligands localized to CNV-associated macrophages and the retinal pigment epithelium/choroid complex. Intravitreal injection of neutralizing antibodies against vascular endothelial growth factor receptor 2, CCR3, CC chemokine ligand 11/eotaxin-1, and CC chemokine ligand 24/eotaxin-2 all reduced CNV area and lesion number in these mice. Systemic administration of the CCR3 antagonists GW766994X and GW782415X reduced spontaneous CNV in JR5558 mice and laser-induced CNV in mouse and primate models in a dose-dependent fashion. Combination treatment with antivascular endothelial growth factor receptor 2 antibody and GW766994X yielded additive reductions in CNV area and hyperpermeability in mice. Interestingly, topical GW766994X and intravitreal anti-CCR3 antibody yielded strong systemic effects, reducing CNV in the untreated, contralateral eye. Contrarily, ocular administration of GW782415X in primates failed to substantially elevate plasma drug levels or to reduce the development of grade IV CNV lesions. These findings suggest that CCR3 signaling may be an attractive therapeutic target for CNV, utilizing a pathway that is at least partly distinct from that of vascular endothelial growth factor receptor. The findings also demonstrate that systemic exposure to CCR3 antagonists may be crucial for CNV-targeted activity.
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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.