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Retinopathy often refers to retinal vascular disease or damage to the retina caused by abnormal blood flow. Retinopathy can be broadly categorized into proliferative and non-proliferative types. Retinopathy is usually an ocular manifestation of systemic disease as seen in diabetes or hypertension. Diabetic retinopathy is the leading cause of blindness in working-aged people. It accounts for around 5% of blindness worldwide and is designated a priority eye disease by the World Health Organization.
Cellular inflammation at the blood–microvascular endothelial cell interface is a common feature of retinal diseases characterized by hyperpermeability and neovascularization. Recent studies in models of ischemic retinopathy show that inflammatory reactions play an important role in initiating vascular injury and dysfunction. Various chemokines and cytokines, such as interleukin (IL)-6, tumor necrosis factor (TNF)-, vascular endothelial cell growth factor (VEGF) and monocyte chemotactic protein (MCP)-1 are upregulated in ischemic retinopathy and have been reported to cause pathologic inflammatory reactions. The increase in inflammatory mediators leads to increased endothelial cell expression of adhesion molecules, including platelet endothelial cell adhesion molecule (PECAM), intercellular adhesion molecule (ICAM)-1 and accumulation of adherent leukocytes in the retinal blood vessels (leukostasis). Stasis of leukocytes and their activation are thought to contribute to the increase in vascular permeability and subsequent neovascularization.
These cytokines trigger several signaling pathways and are largely responsible for the two main sight-threatening complications of diabetic retinopathy: the effects of retinal neovascularization and macular edema consequent to the breakdown of the blood-retinal barrier in the centre of the retina. However, it is very unlikely that the changes in diabetic retinopathy can be explained by any single factor, so research continues into several pathways that may or may not be directly induced by hyperglycemia. These include the renin-angiotensin pathway, glutamate, the kallikrein-kinin system, erythropoietin and the pathway for advanced glycation end products and the advanced glycation end product receptor (AGE-RAGE pathway). The increasing realization that the pathogenesis underlying diabetic retinopathy and especially diabetic macular edema is multifactorial explains why multiple treatment options may be necessary to combat the prevention and progression of the disease.
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