ArticleThe American journal of pathology2013
Ranibizumab is a potential prophylaxis for proliferative vitreoretinopathy, a nonangiogenic blinding disease.
Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02192970 (Bevacizumab Against Recurrent Retinal Detachment), which is not on this map. Cited by 31 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.
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.
Bevacizumab Against Recurrent Retinal Detachment
Who cites it
31 citing papers in PubMed, 0 citations in OpenAlex.
- MIF inhibition attenuates proliferative vitreoretinopathy pathogenesis and protects the eye in preclinical model.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Article
- Bibliometric analysis of research trends on the epiretinal membrane since 2000.Acta biochimica Polonica · 2026Article
- A multicenter study on rates and risk factors of proliferative vitreoretinopathy in a low-income economy.PloS one · 2025Article
- Preoperative Intravitreal Conbercept Injection Reduced Both Angiogenic and Inflammatory Cytokines in Patients With Proliferative Diabetic Retinopathy.Journal of diabetes research · 2024Article
- Proliferative Vitreoretinopathy: A Reappraisal.Journal of clinical medicine · 2023Review
- Vitreal Concentrations of Vascular Endothelial Growth Factor in Patients with Rhegmatogenous Retinal Detachment.Journal of clinical medicine · 2023Article
- Article
- Upregulation of Neuroinflammatory Protein Biomarkers in Acute Rhegmatogenous Retinal Detachments.Life (Basel, Switzerland) · 2022Article
- Vitreous humor proteome: unraveling the molecular mechanisms underlying proliferative and neovascular vitreoretinal diseases.Cellular and molecular life sciences : CMLS · 2022Review
- Short-TermBioMed research international · 2022Article
- Chalcomoracin prevents vitreous-induced activation of AKT and migration of retinal pigment epithelial cells.Journal of cellular and molecular medicine · 2021Article
- The Role of Intravitreal Anti-VEGF Agents in Rabbit Eye Model of Open-Globe Injury.Journal of ophthalmology · 2021Article
- Immunological biomarkers of the vitreous responsible for proliferative alteration in the different forms of retinal detachment.BMC ophthalmology · 2020Article
- Article
- Characterisation of the inflammatory cytokine and growth factor profile in a rabbit model of proliferative vitreoretinopathy.Scientific reports · 2019Article
- Cytokine profiles of phakic and pseudophakic eyes with primary retinal detachment.Acta ophthalmologica · 2019Article
- Proliferative Vitreoretinopathy: A Review.International ophthalmology clinics · 2019Review
- Repair of primary RRD - comparing pars plana vitrectomy procedure with combined phacovitrectomy with standard foldable intraocular lens implantation.Clinical ophthalmology (Auckland, N.Z.) · 2018Article
- PDGFs and their receptors.Gene · 2017Review
- Suppressive effect of AMP-activated protein kinase on the epithelial-mesenchymal transition in retinal pigment epithelial cells.PloS one · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
Proliferative vitreoretinopathy (PVR) exemplifies a disease that is difficult to predict, lacks effective treatment options, and substantially reduces the quality of life of an individual. Surgery to correct a rhegmatogenous retinal detachment fails primarily because of PVR. Likely mediators of PVR are growth factors in vitreous, which stimulate cells within and behind the retina as an inevitable consequence of a breached retina. Three classes of growth factors [vascular endothelial growth factor A (VEGF-A), platelet-derived growth factors (PDGFs), and non-PDGFs (growth factors outside of the PDGF family)] are relevant to PVR pathogenesis because they act on PDGF receptor α, which is required for experimental PVR and is associated with this disease in humans. We discovered that ranibizumab (a clinically approved agent that neutralizes VEGF-A) reduced the bioactivity of vitreous from patients and experimental animals with PVR, and protected rabbits from developing disease. The apparent mechanism of ranibizumab action involved derepressing PDGFs, which, at the concentrations present in PVR vitreous, inhibited non-PDGF-mediated activation of PDGF receptor α. These preclinical findings suggest that available approaches to neutralize VEGF-A are prophylactic for PVR, and that anti-VEGF-based therapies may be effective for managing more than angiogenesis- and edema-driven pathological conditions.
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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.