Abstract
Neovascularization plays an important role in the pathogenesis of a number of ophthalmic disorders, including proliferative diabetic retinopathy and age-related macular degeneration.1 Clinical studies have demonstrated that disruption (usually induced by laser) and subsequent repair of the outer retina and choroid can alter the course of both preretinal and subretinal neovascularization in many cases. Traditionally, investigators have conceptualized these events in physical terms—ischemic retina is "obliterated" or subretinal vessels are "coagulated." Other investigators have hypothesized that a specific "growth factor" or "angiogenic factor" is responsible for the development of new blood vessels and that laser treatment has its effect by destroying cells that produce this factor. Newer evidence strongly suggests that new blood vessel formation occurs in response to a change in the relative balance among a group of "extracellular modulating factors" (EMFs) that are secreted by cells within the retina and adjacent tissue. These extracellular modulating factors control