ArticleBiochimica et biophysica acta. Molecular basis of disease2018
Suppression of aberrant choroidal neovascularization through activation of the aryl hydrocarbon receptor.
Article in Biochimica et biophysica acta. Molecular basis of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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.
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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
14 citing papers in PubMed, 20 citations in OpenAlex.
- Potential therapeutic targets for age-related macular degeneration: The nuclear option.Progress in retinal and eye research · 2023Review
- CD68: Potential Contributor to Inflammation and RPE Cell Dystrophy.Advances in experimental medicine and biology · 2023Review
- Characterization and identification of measurable endpoints in a mouse model featuring age-related retinal pathologies: a platform to test therapies.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Article
- Comparative ligandomics implicates secretogranin III as a disease-restricted angiogenic factor in laser-induced choroidal neovascularization.The FEBS journal · 2022Article
- Gene Delivery of a Caspase Activation and Recruitment Domain Improves Retinal Pigment Epithelial Function and Modulates Inflammation in a Mouse Model with Features of Dry Age-Related Macular Degeneration.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2022Article
- Osteopontin accumulates in basal deposits of human eyes with age-related macular degeneration and may serve as a biomarker of aging.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2022Article
- More than Meets the Eye: The Aryl Hydrocarbon Receptor is an Environmental Sensor, Physiological Regulator and a Therapeutic Target in Ocular Disease.Frontiers in toxicology · 2022Review
- The effect of long-term systemic immunosuppressive drug use on druse formation: a new perspective to age-related macular degenerationTurkish journal of medical sciences · 2020Article
- The Aryl Hydrocarbon Receptor: A Mediator and Potential Therapeutic Target for Ocular and Non-Ocular Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Aryl Hydrocarbon Receptor (AHR) Ligands as Selective AHR Modulators (SAhRMs).International journal of molecular sciences · 2020Review
- Establishing a mouse model of choroidal neovascularization to study the therapeutic effect of levotinib and its mechanism.Saudi journal of biological sciences · 2020Article
- Cell Line Authentication in Vision Research and Beyond: A Tale Retold.Investigative ophthalmology & visual science · 2020Article
- Leveraging Nuclear Receptors as Targets for Pathological Ocular Vascular Diseases.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The aryl hydrocarbon receptor (AhR) is a ligand activated transcription factor, initially discovered for its role in regulating xenobiotic metabolism. There is extensive evidence supporting a multi-faceted role for AhR, modulating physiological pathways important in cell health and disease. Recently we demonstrated that the AhR plays a role in the pathogenesis of age-related macular degeneration (AMD), the leading cause of vision loss in the elderly. We found that loss of AhR exacerbates choroidal neovascular (CNV) lesion formation in a murine model. Herein we tested the therapeutic impact of AhR activation on CNV lesion formation and factors associated with aberrant neovascularization. We screened a panel of synthetic drugs and endogenous AhR ligands, assessed their ability to activate AhR in choroidal endothelial cells, and inhibit angiogenesis in vitro. Drugs with an anti-angiogenic profile were then administered to a murine model of CNV. Two compounds, leflunomide and flutamide, significantly inhibited CNV formation concurrent with positive modifying effects on angiogenesis, inflammation, extracellular matrix remodeling, and fibrosis. These results validate the role of the AhR pathway in regulating CNV pathogenesis, identify mechanisms of AhR-based therapies in the eye, and argue in favor of developing AhR as a drug target for the treatment of neovascular AMD.
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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.