Deconstructing endothelial dysfunction: soluble guanylyl cyclase oxidation and the NO resistance syndrome.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 16955136.
- Also identified by PMC identifier 1555666.
- No licence information is recorded for this record.
- Because redistribution is not established, this page shows the abstract only. Follow the links below for the full text.
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.
Medical subject headings
- Benzoates
- Endothelium, Vascular
- Guanylate Cyclase
- Receptors, Cytoplasmic and Nuclear
- Vasodilation