NOS3 and endothelial dysfunction: In this study, enhanced levels of glomerular nitrotyrosine and the upregulation of endothelial NO synthase (eNOS) by EC-NOX5 expression suggest that superoxide derived from EC-NOX5 potentially utilizes endothelial NO to form nitrotyrosine, leading to the diminished bioavailability of NO, thus causing endothelial dysfunction followed by the promotion of renal injury in diabetes.