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Complex mechanisms act as toothed-wheels of a machine in the ethiopathogenesis of retinal vascular diseases. Although important parts of these mechanisms have been clarified, contributions of some mechanisms are still being studied. Two mechanisms of them are hypoxia and inflammation. Hypoxia has most important role in the manifestations of critical clinicopathological findings of retinal vascular diseases such as retinopathy of prematurity, vascular occlusions and diabetic retinopathy, in addition to its suggested role in the pathogenesis of age-related macular degeneration. Hipoxia-inducible factor 1α (HIF-1α) as a transcription factor, mediates pathogenic mechanisms developing with hypoxia in retina. On the other hand, we observe that inflammatory events take place in certain steps of pathogenesis in retinal vascular diseases as well as age-related macular degeneration. Diabetic retinopathy shows most of the characteristics of an inflammatory disease. Diabetic retinal vascular leakage, capillary nonperfusion, and endothelial cell damage are temporary and spatially associated with retinal leukocyte stasis in early experimental diabetes. Inflammatory mediators are upregulated in diabetic retinopathy and diabetic retinal pathology can be inhibited by anti-inflammatory agents. Vascular endothelial growth factor is key mediator even in the enflamatuar changes of diabetic retina. Conclusively, a body of data generated from experimental diabetes studies indicating that diabetic retinopathy is a low-grade inflammatory disease. However, more work needed to directly prove this hypothesis especially in human diabetic retinopathy. The roles of hypoxia and inflammation in the pathogenesis of retinal vascular diesases as well age-related macular degeneration has been attempted to give substantially in this review article. Keywords : Hypoxia, inflammation, retinal diseases, pathogenesis