Metabolic correlations between kidney and eye in a mouse model of oxygen-induced retinopathy and retinopathy of prematurity

Abstract

Introduction Retinopathy of prematurity (ROP) is one of the leading causes of babies' visual impairment and blindness. There is no effective prevention and treatment of ROP so far, and the shared genetic and developmental similarities among the brain, kidneys and retina may offer novel potential therapeutic approaches to ROP. Objectives The aim of this study is to explore a correlation of ROP patients and the renal, eye tissue of the mouse model of oxygen-induced retinopathy (OIR). Methods and analysis We used renal and vitreous untargeted/targeted metabolomics in OIR to conduct our study. Network association analysis and machine learning were performed with the above results and previous studies: retinal-targeted metabolomics of OIR and human blood-targeted metabolomics of ROP. Results OIR results in retinal neovascularisation and renal injury. Nine canonical signalling pathways were enriched, which are involved in the initiation and progression of pathologic retinal neovascularisation. Arginine biosynthesis emerged as a common pathway across renal, vitreous, retinal and blood metabolomics, suggesting its potential as a predictive biomarker and therapeutic target for ROP and neonatal kidney injury. Conclusion The presence of renal injury-related indicators may assist in diagnosing retinal neovascular diseases such as ROP. Arginine biosynthesis is the best common pathway of kidney-untargeted OIR metabolomics, vitreous- and retina-targeted OIR metabolomics and blood-targeted metabolomics of ROP, indicating that arginine biosynthesis might be the common pathway of ROP and neonatal kidney injury.