NADPH Oxidase 4 at the Nexus of Diabetes, Reactive Oxygen Species, and Renal Metabolism

TL;DRAbstract

NADPH oxidases (NOXs) catalyze the transfer of electrons from NADPH to molecular oxygen to produce superoxide and/or hydrogen peroxide, two major reactive oxygen species (ROS).1 Clarity on in vivo function and relevance to human disease are best exemplified by NOX2, which is responsible for generating the respiratory burst (i.e., large quantities of microbicidal ROS) in phagocytes. In turn, NOX2 deficiency is a cause of chronic granulomatous disease, an inherited disorder characterized by recurrent and persistent infections. Whereas NOX2 and its function within phagosomes were the first to be discovered and are the most widely recognized, in total, seven NOXs have been identified (NOX1, -2, -3, -4, and -5 and dual oxidase 1 and -2) with differences in tissue distribution, intracellular localization, and regulation. In addition to their potential contribution to oxidant stress, NOX ROS production is now recognized to play a fundamental role in cell signaling, with diverse effects on cel

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