الفهرس 
Macular EdemaOnly 14 pages are availabe for public view
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Abstract
Recent studies have demonstrated that VEGF is an important mediator of blood–retinal-barrier breakdown, leading to fluid leakage below the macula and inducing the development of macular edema.
Anti-VEGF agents interfere with receptor binding, thus inhibiting VEGF’s signal, which results in inhibition of abnormal blood vessel formation and decreased vascular permeability. Anti- VEGFs have significant roles in the treatment of many retinal diseases as age related macular degeneration, myopic choroidal neovascularization, proliferative diabetic retinopathy, diabetic macular edema, retinal vein occlusion.
VEGF and its receptors are present in the corneal epithelium, stroma and endothelium, so anti-VEGF therapies may affect the cornea. VEGF plays an important role in stimulating and maintaining corneal neovascularization, and anti-VEGF agents are effective in treating corneal neovascularization.
With the expanding therapeutic applications of anti-VEGF, it is mandatory to investigate the safety profile of anti-VEGFs treatment when used with different modalities. In particular, the cornea may be impaired by direct exposure to high concentration of anti-VEGFs. In vitro VEGF inhibition induces cytotoxic effects on corneal fibroblasts and epithelium.
A recent report demonstrated that the side effects induced by anti-VEGF treatment, including apoptosis mediated by the inhibition of nerve growth factor (NGF) pathway. NGF, the founder of the neurotrophin family, exerts a trophic support not only to the neuronal cells but also to cells of the ocular surface, including corneal epithelium, fibroblasts, and endothelium. NGF plays a key role in the corneal trophism and healing process.