Abstract
Retinopathy of prematurity is a potentially blinding disease associated with low gestational age and birth weight. Suppression of growth factors due to hyperoxia and loss of maternal-fetal interaction cause impaired development of retinal vascularization. Subsequently, an increase in metabolic demands and inadequate vascularization lead to hypoxia that triggers the pathologic neovascularization process, which may lead to a retinal detachment in retinal tissue. Vascular endothelial growth factor (VEGF) has a key role in both physiologic and pathologic vascularization. Based upon in animal models of oxygen-induced retinopathy (OIR) exogenous factors like oxygen levels, oxidative stress, inflammation and cytokines, several signaling pathways and receptors have been linked to the pathogenesis of retinopathy of prematurity.
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