ReviewSeminars in immunopathology2008
Angiogenesis in eye disease: immunity gained or immunity lost?
Review in Seminars in immunopathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
28 citing papers in PubMed, 46 citations in OpenAlex.
- AIP1 Regulates Ocular Angiogenesis Via NLRP12-ASC-Caspase-8 Inflammasome-Mediated Endothelial Pyroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Role of macrophage in ocular neovascularization.Heliyon · 2024Review
- Article
- MacrophageLife science alliance · 2023Article
- Ocular injury progression and cornea histopathology from chloropicrin vapor exposure: Relevant clinical biomarkers in mice.Experimental eye research · 2023Article
- Neurodevelopmental outcome of infants who develop necrotizing enterocolitis: The gut-brain axis.Seminars in perinatology · 2023Article
- Targeting Neurovascular Interaction in Retinal Disorders.International journal of molecular sciences · 2020Review
- Cholesterol homeostasis, macrophage malfunction and age-related macular degeneration.Annals of translational medicine · 2018Article
- Retinal Vasculature in Development and Diseases.Annual review of vision science · 2018Review
- Doyne lecture 2016: intraocular health and the many faces of inflammation.Eye (London, England) · 2017Review
- Overexpression of Soluble Fas Ligand following Adeno-Associated Virus Gene Therapy Prevents Retinal Ganglion Cell Death in Chronic and Acute Murine Models of Glaucoma.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Targeted complement inhibition and microvasculature in transplants: a therapeutic perspective.Clinical and experimental immunology · 2016Review
- Thrombospondin-1-Based Antiangiogenic Therapy.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2015Article
- A chimeric Cfh transgene leads to increased retinal oxidative stress, inflammation, and accumulation of activated subretinal microglia in mice.Investigative ophthalmology & visual science · 2015Article
- The retinal pigment epithelium (RPE) induces FasL and reduces iNOS and Cox2 in primary monocytes.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2014Article
- Aging is not a disease: distinguishing age-related macular degeneration from aging.Progress in retinal and eye research · 2013Review
- Islet inflammation in plain sight.Diabetes, obesity & metabolism · 2013Review
- Overexpression of membrane-bound fas ligand (CD95L) exacerbates autoimmune disease and renal pathology in pristane-induced lupus.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Age-dependent changes in FasL (CD95L) modulate macrophage function in a model of age-related macular degeneration.Investigative ophthalmology & visual science · 2013Article
- Peptidoglycan and muramyl dipeptide from Staphylococcus aureus induce the expression of VEGF-A in human limbal fibroblasts with the participation of TLR2-NFκB and NOD2-EGFR.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The anti-inflammatory nature of the intraocular environment is critical to the immune privilege of the eye. An important part of immune privilege is the induction of apoptosis by two death-inducing ligands (FasL and TRAIL) that can limit the spread of inflammation and control tumor growth. While initial studies focused on control of inflammation and the impact of these molecules on the systemic immune response, more recent studies have extended this concept to pathogenic neovascularization. This process is an important component of several blinding eye disorders including age-related macular degeneration, diabetic retinopathy, retinopathy of prematurity, and corneal disease. These studies showed that the mediators of immune privilege also regulate the extent of angiogenesis. In this article, we will develop the idea that constitutive expression of FasL in the eye, as well as inducible FasL on cells of the immune system, modulates neovascularization in ocular disease. Further, we will present the idea that macrophage participation in this process and their function during disease depends on the microenvironment and the cytokine milieu. These concepts challenge the idea that neovascular eye disease is simply an inflammatory process and support the idea that these diseases may result from the loss or dysfunction of important components of the cellular immune system.
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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.