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M Lang, B Kojonazarov, X Tian, A Kalymbetov, N Weissmann, F Grimminger, A Kretschmer, JP Stasch, W Seeger, HA Ghofrani and RT Schermuly
Abstract
The nitric oxide (NO)-soluble guanylate cyclase (sGC)-cyclic guanosine monophosphate (cGMP) signal-transduction pathway is impaired in many cardiovascular diseases, including pulmonary arterial hypertension (PAH). Riociguat (BAY 63-2521) is a stimulator of sGC that works both in synergy with and independently of NO to increase levels of cGMP. The aims of this study were to investigate the role of NO-sGC-cGMP signaling in a model of severe PAH and to evaluate the effects of sGC stimulation by riociguat and PDE5 inhibition by sildenafil on pulmonary hemodynamics and vascular remodeling in severe experimental PAH.
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Concepts
Pulmonology, Myocardial infarction, Pulmonary artery, Sildenafil, Riociguat, Guanylate cyclase, Nitric oxide, Pulmonary hypertension
MeSH headings
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