cxcr3 antagonism of sdf-1(5-67) restores trabecular function and prevents retinal neurodegeneration in a rat model of ocular hypertensioncxcr3 sdf-1拮抗作用(5 - 67)恢复小梁功能和防止视网膜神经退化在眼部的高血压大鼠模型.pdfVIP
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cxcr3 antagonism of sdf-1(5-67) restores trabecular function and prevents retinal neurodegeneration in a rat model of ocular hypertensioncxcr3 sdf-1拮抗作用(5 - 67)恢复小梁功能和防止视网膜神经退化在眼部的高血压大鼠模型
CXCR3 Antagonism of SDF-1(5-67) Restores Trabecular Function and Prevents Retinal Neurodegeneration in a Rat Model of Ocular Hypertension 1,2,3,4 1,2,3 ´ ´ 5 1,2,3 1,2,3 Alexandre Denoyer *, David Godefroy , Isabelle Celerier , Julie Frugier , Julie Degardin , 6 1,2,3,7 1,2,3 8 Jeffrey K. Harrison , Francoise Brignole-Baudouin , Serge Picaud , Francoise Baleux , ´ 1,2,3,4 ` 1,2,3. 1,2,3,4. Jose A. Sahel , William Rostene , Christophe Baudouin 1 UPMC University Paris 6, Institut de la Vision, UMRS968, Paris, France, 2 INSERM, U968, Paris, France, 3 CNRS, U7210, Paris, France, 4 Quinze-Vingts National Ophthalmology Hospital, Paris, France, 5 Team 1, Centre de Recherche des Cordeliers, INSERM, U872, Paris, France, 6 Department of Pharmacology Therapeutics, College of Medicine, University of Florida, Gainesville, Florida, United States of America, 7 Department of Toxicology, Faculty of Biological and Pharmacological Sciences, University ´ ´ ´ Rene Descartes Paris 05, Paris, France, 8 Unite de chimie des biomolecules, Institut Pasteur, CNRS 2128, Paris, France Abstract Glaucoma, the most common cause of irreversible blindness, is a neuropathy commonly initiated by pathological ocular hypertension due to unknown mechanisms of trabecular meshwork degeneration. Current antiglaucoma therapy does not target the causal trabecular pathology, which may explain why treatment fa
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