Summary of project PR002157

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR002157. The data can be accessed directly via it's Project DOI: 10.21228/M8T24J This work is supported by NIH grant, U2C- DK119886. See: https://www.metabolomicsworkbench.org/about/howtocite.php

Project ID: PR002157
Project DOI:doi: 10.21228/M8T24J
Project Title:Exogenous L-serine supply protects against retinopathy of prematurity in a murine model
Project Summary:Pathological retinal angiogenesis with irregular and fragile vessels (also termed as neovascularization, a response to hypoxia and dysmetabolism) is a leading cause of vision loss in all age groups driven in part by unmet metabolic demand from retinal neurons. Sustaining neural retinal metabolism with an adequate nutrient supply may prevent vision-threatening neovascularization. Low circulating serine levels are associated with neovascularization in macular telangiectasia and altered serine/glycine metabolism is suggested in retinopathy of prematurity. Here we assessed the role of serine metabolism in suppressing hypoxia-driven retinal neovascularization in mice. Serine or vehicle control was supplemented systemically via intraperitoneal injection. Systemic serine supplementation decreased retinal neovascularization. Metabolomic analysis showed serine treatment increased metabolites involved in fatty acid oxidation and phospholipid synthesis.
Institute:Boston Children's Hospital
Last Name:Fu
First Name:Zhongjie
Address:1 Blackfan Circle, Boston, MA 02114
Email:Zhongjie.Fu@childrens.harvard.edu
Phone:617-919-2534

Summary of all studies in project PR002157

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ST003512 Exogenous L-serine supply protects against retinopathy of prematurity in a murine model Mus musculus Boston Children's Hospital MS 2025-05-01 1 15 Uploaded data (343.8M)*
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