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More weapons in the arsenal against ischemic retinopathy.

Ischemia-induced retinopathy is the major cause of blindness world-wide. Diverse processes may lead to retinal ischemia, including a central retinal vein occlusion, a progressive deterioration of vascular function due to prolonged hyperglycemia, and obliteration of newly formed retinal vessels in premature neonates subjected to hyperoxia. The later two processes may culminate in the development of proliferative diabetic retinopathy (PDR) and retinopathy of prematurity (ROP), respectively. While different etiologies may lead to insufficient perfusion of the retina, once a critical level of ischemia has been achieved, the different forms of retinopathy seem to converge on a common sequela — the hypoxia-induced formation of morphologically abnormal vessels. Retinopathy-associated neovascularization is excessive and neo-vessels are abnormally leaky and tend to breach the inner limited membrane of the retina and invade the vitreous. Such pre-retinal vascular growth is perhaps the most devastating aspect of retinopathy, as it often leads to retina detachment and eventually to blindness. 
 
Combating retinopathy can, in principle, be directed against the first pathogenic phase, the generation of a vascular deficit and the resultant ischemia, or against the second phase, the formation of surplus, abnormal vessels. At least for PDR, the former approach has been impossible because we lack sufficient insight into the mechanisms leading to progressive vessel dysfunction, or even a suitable animal model in which to study these events. For this reason, most of the studies outlined below have resorted to the use of an oxygen-induced retinopathy model (i.e., an ROP model) (1).