Abstract

Retinopathy of prematurity (ROP) is a clinically multifactorial process characterized by the aberrant vascularization of the retina that has potentially devastating effects on vision in preterm infants. Despite an appreciation for the postnatal risk factors that contribute to the development of ROP, this condition continues to be a major cause of childhood blindness. Studies using the mouse model of oxygen-induced retinopathy (OIR) have identified new therapeutic targets that may be used to guide treatment and determine which babies are at highest risk for ROP development. Such factors include the hypoxia-driven proteins vascular endothelial growth factor (VEGF) and erythropoietin (EPO) as well as the maternally derived factors insulin-like growth factor-1 (IGF-1) and omega-3 polyunsaturated fatty acids (PUFAs). Each has been demonstrated to have phase-specific effects on the pathogenesis of ROP. Through an understanding of the contribution of the IGF-1 pathway to the development of ROP in particular, a new algorithm has been developed (WINROP™) that uses postnatal weight gain to identify infants at highest risk for ROP in an attempt to target therapy and resources more effectively.

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