Retinal neovascularization, the second phase of ROP, is hypoxia-induced [11, 45] and occurs between roughly 32 and 34 weeks PMA. The neovascularization phase of ROP is similar to other proliferative retinopathies such as diabetic retinopathy. The new blood vessel formation occurs at the junction between the nonvascular-ized retina and the vascularized retina. These new vessels are leaky and can cause tractional retinal detachments leading to blindness. If we could allow the normal growth of blood vessels after preterm birth, the second destructive phase would not occur. Alternatively, if we could attenuate the rapid proliferation of abnormal blood vessels in the second phase and allow controlled vascularization of the retina, retinal detachments could be prevented.
To accomplish these goals, it is necessary to understand the growth factors involved in all aspects of ROP, both in normal retinal vascular development and in the development of neovas-
cularization. The two phases of ROP are mirror images. The first involves growth inhibition of neural retina and the retinal vasculature, and the second involves uncontrolled proliferative growth of retinal blood vessels. The controlling growth factors are likely to be deficient in phase I and in excess in phase II. Therefore control of the disease is likely to be complex and will likely require careful timing of any intervention.
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