Abstract
The hallmark feature of the wet or neovascular form of age-related macular degeneration is the presence of choroidal (or retinal) neovascularization (CNV). If left untreated, CNV may result in significant central vision loss due to complications including exudation, leakage, and ultimately subretinal fibrosis causing remarkable photoreceptor loss. Although the mechanism of development is not fully understood, the process of neovascularization is driven by the upregulation of angiogenic cytokines, principally vascular endothelial growth factor (VEGF). Inhibition of VEGF with intravitreal anti-VEGF therapy has become the standard of care for macular CNV, helping to prevent legal blindness in millions of affected patients worldwide.
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