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. Author manuscript; available in PMC: 2017 Aug 1.
Published in final edited form as: Biochim Biophys Acta. 2016 May 4;1862(8):1392–1400. doi: 10.1016/j.bbadis.2016.05.002

Figure 4.

Figure 4

Progression of retinopathy of prematurity. Retinal blood vessels grow normally in utero (low oxygen tension). After premature birth, the retinal vasculature is incomplete and vascularization is inhibited (Phase 1), due to the hyperoxic exposure that maintains the adequate circulating oxygen levels to keep the infants survive. As the retina matures, metabolic demand is increased, leading to the localized hypoxia which in turn stimulates the oxygen-regulated angiogenic factors to induce retinal neovascularization.