The vascular beds supplying the retina may sustain injury as a result of underlying disease such as diabetes, and/or the interaction of
genetic predisposition, environmental insults, and age. The vascular pathologic features observed in different intraocular
vascular diseases can be categorized broadly as proliferation, exemplified by proliferative
diabetic retinopathy, leakage such as
macular edema secondary to
retinal vein occlusion, or a combination of proliferation and leakage, as seen in neovascular
age-related macular degeneration (AMD). The World Health Organization has identified
diabetic retinopathy and AMD as priority
eye diseases for the prevention of vision loss in developed countries. The pathologic transformations of the retinal vasculature seen in intraocular
vascular disease are associated with increased expression of
vascular endothelial growth factor A (
VEGF), a potent endothelial-specific
mitogen. Furthermore, in model systems,
VEGF alone is sufficient to trigger intraocular neovascularization, and its inhibition is associated with functional and anatomic improvements in the affected eye. Therapeutic interventions with effect on
VEGF include intraocular capture and neutralization by engineered
antibodies or chimeric receptors, downregulation of its expression with
steroids, or alleviation of
retinal ischemia, a major stimulus for
VEGF expression, with
retinal ablation by
laser treatment. Data from prospective randomized clinical trials indicate that
VEGF inhibition is a potent therapeutic strategy for intraocular
vascular disease. These findings are changing clinical practice and are stimuli for further study of the basic mechanisms controlling intraocular angiogenesis.
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