ArticleNature2009
CCR3 is a target for age-related macular degeneration diagnosis and therapy.
Article in Nature, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers, 1 of them a synthesis that pooled it.
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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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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.
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Who cites it
139 citing papers in PubMed, 1 synthesis or guideline pooled it, 256 citations in OpenAlex.
- Quantum Dots in Ocular Surface: A Systematic Review.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnologyPooled it
- Leukocytes and age-related macular degeneration.European journal of epidemiology · 2026Article
- People living with lower extremity peripheral artery disease demonstrate vascular regenerative cell deficiencies: The PAD-VRCE CardioLink-17 study.JVS-vascular science · 2026Article
- Circulating Inflammatory Proteins and Age-related Macular Degeneration: New Insights from Mendelian Randomization.Combinatorial chemistry & high throughput screening · 2026Article
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- CCL11 released by GSDMD-mediated macrophage pyroptosis regulates angiogenesis after hindlimb ischemia.Cell death discovery · 2024Article
- Therapeutic targeting of telomerase ameliorates experimental choroidal neovascularization.Biochimica et biophysica acta. Molecular basis of disease · 2024Article
- Role of microglia/macrophage polarisation in intraocular diseases (Review).International journal of molecular medicine · 2024Review
- Chemokine Receptor Profile of T Cells and Progression Rate of Geographic Atrophy Secondary to Age-related Macular Degeneration.Investigative ophthalmology & visual science · 2024Observational
- CCR3 Expression in Relation to Delayed Microbleeds in a Rat Model of Large Vessel Occlusion.Journal of experimental neurology · 2024Article
- Oral Metformin Inhibits Choroidal Neovascularization by Modulating the Gut-Retina Axis.Investigative ophthalmology & visual science · 2023Article
- Ocular Vascular Diseases: From Retinal Immune Privilege to Inflammation.International journal of molecular sciences · 2023Review
- Profiling disease-selective drug targets: From proteomics to ligandomics.Drug discovery today · 2023Review
- Rethinking the potential and necessity of drug delivery systems in neovascular age-related macular degeneration therapy.Frontiers in bioengineering and biotechnology · 2023Review
- Editorial: Molecular imaging in retinal diseases.Frontiers in medicine · 2023Article
- Retinal fluid is associated with cytokines of aqueous humor in age-related macular degeneration using automatic 3-dimensional quantification.Frontiers in cell and developmental biology · 2023Article
- Dimethyl Fumarate Protects Retinal Pigment Epithelium from Blue Light-Induced Oxidative Damage via the Nrf2 Pathway.Antioxidants (Basel, Switzerland) · 2022Article
- IL-4 induces reparative phenotype of RPE cells and protects against retinal neurodegeneration via Nrf2 activation.Cell death & disease · 2022Article
- Fecal microbiota transfer between young and aged mice reverses hallmarks of the aging gut, eye, and brain.Microbiome · 2022Article
79 more citing papers are in PubMed but not listed here.
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Authors and funding
27 authors at 9 institutions in 3 countries.
Funding
Abstract
Age-related macular degeneration (AMD), a leading cause of blindness worldwide, is as prevalent as cancer in industrialized nations. Most blindness in AMD results from invasion of the retina by choroidal neovascularisation (CNV). Here we show that the eosinophil/mast cell chemokine receptor CCR3 is specifically expressed in choroidal neovascular endothelial cells in humans with AMD, and that despite the expression of its ligands eotaxin-1, -2 and -3, neither eosinophils nor mast cells are present in human CNV. Genetic or pharmacological targeting of CCR3 or eotaxins inhibited injury-induced CNV in mice. CNV suppression by CCR3 blockade was due to direct inhibition of endothelial cell proliferation, and was uncoupled from inflammation because it occurred in mice lacking eosinophils or mast cells, and was independent of macrophage and neutrophil recruitment. CCR3 blockade was more effective at reducing CNV than vascular endothelial growth factor A (VEGF-A) neutralization, which is in clinical use at present, and, unlike VEGF-A blockade, is not toxic to the mouse retina. In vivo imaging with CCR3-targeting quantum dots located spontaneous CNV invisible to standard fluorescein angiography in mice before retinal invasion. CCR3 targeting might reduce vision loss due to AMD through early detection and therapeutic angioinhibition.
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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.