ArticleInvestigative ophthalmology & visual science2013
Aurintricarboxylic acid inhibits complement activation, membrane attack complex, and choroidal neovascularization in a model of macular degeneration.
Article in Investigative ophthalmology & visual science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- The Role of Osteopontin in Microglia Biology: Current Concepts and Future Perspectives.Biomedicines · 2022Review
- Novel approach to antiangiogenic factors in age-related macular degeneration therapy.Central-European journal of immunology · 2022Review
- Molecular Mechanisms of Retinal Pigment Epithelium Dysfunction in Age-Related Macular Degeneration.International journal of molecular sciences · 2021Review
- The role of complement in brain injury following intracerebral hemorrhage: A review.Experimental neurology · 2021Review
- Discovery ofMicroorganisms · 2021Article
- Retinal pigment epithelium and age-related macular degeneration: A review of major disease mechanisms.Clinical & experimental ophthalmology · 2020Review
- The role of lymphocytes and phagocytes in age-related macular degeneration (AMD).Cellular and molecular life sciences : CMLS · 2020Review
- Complement Inhibition Attenuates Early Erythrolysis in the Hematoma and Brain Injury in Aged Rats.Stroke · 2019Article
- Modulation of three key innate immune pathways for the most common retinal degenerative diseases.EMBO molecular medicine · 2018Review
- Imidazole Compounds for Protecting Choroidal Endothelial Cells from Complement Injury.Scientific reports · 2018Article
- New insight into the role of the complement in the most common types of retinopathy-current literature review.International journal of ophthalmology · 2018Review
- From compliment to insult: genetics of the complement system in physiology and disease in the human retina.Human molecular genetics · 2017Review
- A novel bispecific molecule delivered by recombinant AAV2 suppresses ocular inflammation and choroidal neovascularization.Journal of cellular and molecular medicine · 2017Article
- Screening of a composite library of clinically used drugs and well-characterized pharmacological compounds for cystathionine β-synthase inhibition identifies benserazide as a drug potentially suitable for repurposing for the experimental therapy of colon cancer.Pharmacological research · 2016Article
- Targeting the complement system for the management of retinal inflammatory and degenerative diseases.European journal of pharmacology · 2016Review
- Tenascin-C promotes angiogenesis in fibrovascular membranes in eyes with proliferative diabetic retinopathy.Molecular vision · 2016Article
- Topical application of a G-Quartet aptamer targeting nucleolin attenuates choroidal neovascularization in a model of age-related macular degeneration.Experimental eye research · 2015Article
- Complement activation and choriocapillaris loss in early AMD: implications for pathophysiology and therapy.Progress in retinal and eye research · 2015Review
- Age-Related Macular Degeneration: A Disease of Systemic or Local Complement Dysregulation?Journal of clinical medicine · 2014Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
purposeImmunocytochemical and genetic data implicate a significant role for the activation of complement in the pathology of AMD. Individuals homozygous for a Y402H polymorphism in Factor H have elevated levels of membrane attack complex (MAC) in their choroidal blood vessels and RPE relative to individuals homozygous for the wild-type allele. An R95X polymorphism in C9, a protein necessary for the final assembly of MAC, is partially protective against the formation of choroidal neovascularization (CNV) in AMD patients. Aurintricarboxylic Acid (ATA) is a small molecule inhibitor of MAC. Our hypothesis was that attenuation of the formation of MAC on ocular tissues by ATA may protect mice against laser-induced CNV.
methodsThe ability of ATA to inhibit human complement-mediated cell lysis, inhibit formation of human MAC, and inhibit formation of tubes by endothelial cells was examined in vitro. Subsequently, the Bruch's membrane of adult mice was damaged using an argon laser, followed by intravitreal injection of ATA. One week later, choroidal flat mounts from these mice were stained for the presence of MAC, endothelial cells, and macrophages.
resultsATA protects cells from human complement-mediated lysis, attenuates assembly of the MAC, and inhibits tube formation by endothelial cells in vitro. ATA also attenuates CNV, MAC deposition, and macrophage infiltration in a murine model of exudative AMD.
conclusionsATA warrants further study as a potential drug for the treatment of exudative and nonexudative AMD.
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Registered trials
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