Abstract

Macular edema is most often clinically defined as an accumulation of serous fluid within the neurosensory retina with increased thickness of the central retina. In exudative age-related macular degeneration the leakage of fluid from the choroidal new vessels may be the origin of macular edema. Their abnormal permeability and the inflammatory reaction are mechanisms involved in this accumulation of fluid, which occurs in all layers. Cystoid macular edema is more often associated with subepithelial occult choroidal neovascularization (CNV) than it is with pre-epithelial classic CNV. The simultaneous presence of choroidal new vessels and ME implies a number of cellular dysfunctions especially of Müller cells and subsequently metabolic alterations. The leakage from the choroidal new vessels, predominantly vascular endothelial growth factor (VEGF)-induced, may produce a large accumulation of fluid under the neurosensory retina. It is also likely that the key signaling steps occur prior to the upregulation of VEGF either initiated by, or facilitated by, cytokines, which act under normal basic conditions to counterbalance the integral VEGF effects and, in pathologic circumstances, may either counteract or serve to amplify the process.

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