Oxidative stress has been linked to the pathogenesis of the major complications of diabetes in the kidney, the heart, the eye or the vasculature. NADPH oxidases of the Nox family are a major source of ROS (reactive oxygen species) and are critical mediators of redox signalling in cells from different organs afflicted by the diabetic milieu. In the present review, we provide an overview of the current knowledge related to the understanding of the role of Nox in the processes that control cell injury induced by hyperglycaemia and other predominant factors enhanced in diabetes, including the renin–angiotensin system, TGF-β (transforming growth factor-β) and AGEs (advanced glycation end-products). These observations support a critical role for Nox homologues in diabetic complications and indicate that NADPH oxidases are an important therapeutic target. Therefore the design and development of small-molecule inhibitors that selectively block Nox oxidases appears to be a reasonable approach to prevent or retard the complications of diabetes in target organs. The bioefficacy of these agents in experimental animal models is also discussed in the present review.
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Review Article| June 14 2013
Nox as a target for diabetic complications
*Department of Medicine, University of Texas Health Science Center, Department of Medicine, San Antonio, TX 78229, U.S.A.
†South Texas Veterans Health Care System, Audie L. Murphy Memorial Hospital Division, San Antonio, TX 78229, U.S.A.
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Yves Gorin, Karen Block; Nox as a target for diabetic complications. Clin Sci (Lond) 1 October 2013; 125 (8): 361–382. doi: https://doi.org/10.1042/CS20130065
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