Abstract
Retinopathy of prematurity is defined as retinal abnormalities that occur during development as a consequence of disturbed oxygen conditions and nutrient supply after preterm birth. Both neuronal maturation and retinal vascularization are impaired, leading to the compensatory but uncontrolled retinal neovessel growth. Current therapeutic interventions target the hypoxia-induced neovessels but negatively impact retinal neurons and normal vessels. Emerging evidence suggests that metabolic disturbance is a significant and underexplored risk factor in the disease pathogenesis. Hyperglycemia and dyslipidemia correlate with the retinal neurovascular dysfunction in infants born prematurely. Nutritional and hormonal supplementation relieve metabolic stress and improve retinal maturation. Here we focus on the mechanisms through which metabolism is involved in preterm-birth-related retinal disorder from clinical and experimental investigations. We will review and discuss potential therapeutic targets through the restoration of metabolic responses to prevent disease development and progression.
Highlights
Most studies assessing the effect of DHA-rich intravenous lipid emulsions have been retrospective comparative studies while only a few have prospectively investigated their role in retinopathy of prematurity (ROP) outcome, which likely contributes to the heterogeneity of the reported results
Results from a recent in preterm suggests that and from a recent pilotpilot studystudy in preterm infantsinfants suggests that enteral enteral supplementation with
Pathological angiogenesis is induced in mouse retinas with low lipid uptake and reduced fatty acid oxidation [3]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. ROP begins with suppression in the growth of immature retinal vasculature As the neural retina slowly matures, the increased metabolic demand for nutrients and oxygen is not met in the avascular retinal region. Hypoxia and nutrient deprivation are driving forces to induce retinal vessel growth [3,4]. These newly-formed vessels are uncontrolled and fragile (phase II ROP). Of essential nutrients and pro-angiogenic afterin birth in combination with sion of high supplemental oxygen, leads to hyperoxia that suppresses retinal vascularization (Phase 1). In the second phase of ROP (Phase 2), relative hypoxia and increased nutrient demands of cular retina drives fibrovascular proliferation. ROP (APROP), rapidly progresses to tractional detachment
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