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Abstract #78944 Published in IGR 20-1
A Metabolomics Profiling of Glaucoma Points to Mitochondrial Dysfunction, Senescence, and Polyamines Deficiency
Leruez S; Marill A; Bresson T; de Saint Martin G; Buisset A; Muller J; Tessier L; Gadras C; Verny C; Gohier P; Amati-Bonneau P; Lenaers G; Bonneau D; Simard G; Milea D; Procaccio V; Reynier P; Chao de la Barca JMInvestigative Ophthalmology and Visual Science 2018; 59: 4355-4361
PURPOSE: To determine the plasma metabolomic signature of primary open-angle glaucoma (POAG). METHODS: We compared the metabolomic profiles of plasma from individuals with POAG (n = 36) with age- and sex-matched controls with cataract (n = 27). A targeted metabolomics study was performed using the standardized p180 Biocrates Absolute IDQ p180 kit with a QTRAP 5500 mass spectrometer. Multivariate analyses were performed using principal component analysis (PCA) and the least absolute shrinkage and selection operator (LASSO) method. RESULTS: Among the 151 metabolites accurately measured, combined univariate and multivariate analyses revealed 18 discriminant metabolites belonging to the carbohydrate, acyl-carnitine, phosphatidylcholine, amino acids, and polyamine families. The metabolomic signature of POAG points to three closely interdependent pathophysiologic conditions; that is, defective mitochondrial oxidation of energetic substrates, altered metabolism resembling that observed in senescence, and a deficiency in spermidine and spermine, both polyamines being involved in the protection of retinal ganglion cells. CONCLUSIONS: Our results highlight a systemic and age-related mitochondrial defect in the pathogenesis of POAG.
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Classification:
3.8 Pharmacology (Part of: 3 Laboratory methods)
9.4.15 Glaucoma in relation to systemic disease (Part of: 9 Clinical forms of glaucomas > 9.4 Glaucomas associated with other ocular and systemic disorders)
