Journal article
NADPH oxidase, NOX1, mediates vascular injury in ischemic retinopathy
JL Wilkinson-Berka, D Deliyanti, I Rana, AG Miller, A Agrotis, R Armani, C Szyndralewiez, K Wingler, RM Touyz, ME Cooper, KA Jandeleit-Dahm, HHHW Schmidt
Antioxidants and Redox Signaling | MARY ANN LIEBERT, INC | Published : 2014
Abstract
Aims: Ischemic retinal diseases such as retinopathy of prematurity are major causes of blindness due to damage to the retinal microvasculature. Despite this clinical situation, retinopathy of prematurity is mechanistically poorly understood. Therefore, effective preventative therapies are not available. However, hypoxic-induced increases in reactive oxygen species (ROS) have been suggested to be involved with NADPH oxidases (NOX), the only known dedicated enzymatic source of ROS. Our major aim was to determine the contribution of NOX isoforms (1, 2, and 4) to a rodent model of retinopathy of prematurity. Results: Using a genetic approach, we determined that only mice with a deletion of NOX1,..
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Awarded by Monash University
Funding Acknowledgements
The authors thank Mariam Sofi and David R. Berka for technical assistance. The authors thank Monash Micro Imaging for assistance with confocal microscopy. JDRF and the NHMRC of Australia generously supported this research. Both J.L.W.-B. and K.A.J.-D. are NHMRC Senior Research Fellows. M. E. C. is an Australian Fellow of the NHMRC and JDRF Scholar. H.H.H.W.-S. is supported by the EU (Marie Curie International Reintegration Grant and ERC Advanced Grant) and Dutch Kidney Foundation. D. D. was awarded a Post-graduate Publication Award from the Monash University.