Retinopathy of prematurity (ROP) is a potentially blinding disorder in premature infants. The underlying pathophysiology is incompletely understood, limiting the prevention and treatment of this devastating condition. Current therapies are directed toward management of aberrant neovascularization thought to result from retinal ischemia in the developing preterm retina. The molecular mediators important for development of retinal ischemia and subsequent neovascular pathology are not fully understood. However, oxygen has been shown to be a key mediator of disease and the oxygen environment for preterm infants has been extensively studied. Despite this, the optimal oxygen environment for preterm infants remains unclear and recent works seeking to clarify this relationship demonstrate somewhat disparate findings. These data further substantiate that ROP is a complex disease with multifactorial etiology including genetic and environmental factors. Therefore, while environmental factors such as oxygen are important to our understanding of the disease process and care of preterm infants, identification of the molecular mediators downstream of oxygen which are necessary for development of ROP pathology will be critical to improve prevention, diagnosis and treatment strategies.
Keywords: Angiogenesis; Neovascularization; Oxygen; Retinopathy of Prematurity (ROP).