Abstract
The article by Sukumar et al. (1) published in a recent issue of Diabetes concludes that the type 2 NADPH oxidase (Nox2) plays a critical role in insulin resistance–related endothelial dysfunction. However, in our opinion it is too premature to draw these conclusions when looking at the entire body of available literature. The authors show in two different genetic mouse models of insulin resistance a blunted endothelium-dependent aortic relaxation to acetylcholine that can be reversed to normal both in vitro and in vivo by applying the peptide gp91ds-tat, which interferes with protein–protein interactions during Nox2 activation. Similarly, knockout …
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