Role of Cytokines and Trophic Factors in the Pathogenesis of Diabetic Retinopathy
Diabetic retinopathy (DR) is one of the most frequent complications of diabetes and the leading cause of acquired blindness in developed countries. A note worthy problem in DR is the formation of fibrovascular epiretinal membranes (ERMs) which can cause tractional retinal detachment in the progressed stage of DR. Ocular vitreous fluid and ERMs, which can be obtained during vitrectomy, allow laboratory studies investigating the pathogenesis of DR. Recent studies have shown a significant association between clinical grades of DR and the expression levels of specific cytokines, such as vascular endothelial growth factor (VEGF), in the intraocular fluid. In addition, expression of various trophic factors and their receptors are reported in ERMs. ERM is composed of many cell types including endothelial cells, which is the primary target of glucose-induced dysfunction in the retina. However, some trophic factor receptors are observed in other cell types such as the glial cells, and their role in ERMs is unclarified. These findings may uncover the detailed pathogenesis of DR, which may lead to new therapeutic strategies. This review briefly summarizes recent research regarding the clinical and laboratory findings of DR.
No Supplementary Data
No Article Media
Document Type: Review Article
Affiliations: Department of Molecular Neurobiology, Tokyo Metropolitan Institute for Neuroscience, 2-6 Musashidai, Fuchu, Tokyo 183-8526, Japan.
Publication date: January 1, 2005
More about this publication?
- Current Diabetes Reviews publishes frontier reviews on all the latest advances on diabetes and its related areas e.g. pharmacology, pathogenesis, complications, epidemiology, clinical care, and therapy.
The journal's aim is to publish the highest quality review articles dedicated to clinical research in the field. The journal is essential reading for all researchers and clinicians who are involved in the field of diabetes.
- Editorial Board
- Information for Authors
- Subscribe to this Title
- Ingenta Connect is not responsible for the content or availability of external websites