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Usage Information

Deconstructing endothelial dysfunction: soluble guanylyl cyclase oxidation and the NO resistance syndrome
Mark T. Gladwin
Mark T. Gladwin
Published September 1, 2006
Citation Information: J Clin Invest. 2006;116(9):2330-2332. https://doi.org/10.1172/JCI29807.
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Commentary

Deconstructing endothelial dysfunction: soluble guanylyl cyclase oxidation and the NO resistance syndrome

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Abstract

In this issue of the JCI, Stasch and colleagues suggest that a novel drug, BAY 58-2667, potently activates a pool of oxidized and heme-free soluble guanylyl cyclase (sGC; see the related article beginning on page 2552). The increased vasodilatory potency of BAY 58-2667 the authors found in a number of animal models of endothelial dysfunction and in human blood vessels from patients with diabetes suggests that there exists a subphenotype of endothelial dysfunction characterized by receptor-level NO resistance. Diseases associated with NO resistance would appear to be ideally suited for therapies directed at restoring redox homeostasis, sGC activity, and NO sensitivity.

Authors

Mark T. Gladwin

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