|1.||Stasch, Johannes-Peter: 7 articles (01/2015 - 04/2005)|
|2.||Murad, Ferid: 6 articles (12/2014 - 09/2003)|
|3.||Martin, Emil: 5 articles (12/2014 - 09/2003)|
|4.||Papapetropoulos, Andreas: 4 articles (06/2015 - 01/2006)|
|5.||Friebe, Andreas: 4 articles (01/2015 - 05/2007)|
|6.||Glynos, Constantinos: 3 articles (06/2015 - 04/2007)|
|7.||Brouckaert, Peter: 3 articles (06/2015 - 10/2013)|
|8.||Sharina, Iraida G: 3 articles (12/2014 - 09/2003)|
|9.||De Nucci, Gilberto: 3 articles (11/2014 - 01/2012)|
|10.||Mónica, Fabíola Z: 3 articles (11/2014 - 01/2012)|
|1.||Acute Kidney Injury (Acute Renal Failure)
08/01/2015 - "The present study investigated the possible involvement of nitric oxide/soluble guanylyl cyclase (NO/sGC) pathway in ascorbic acid (AA)-mediated protection against acute kidney injury (AKI) in rats. "
08/01/2015 - "Investigation of the role of nitric oxide/soluble guanylyl cyclase pathway in ascorbic acid-mediated protection against acute kidney injury in rats."
02/01/2000 - "After simulated in vitro ischemia the activation of soluble guanylyl cyclase by NO is transiently inhibited resulting in a transient anti-apoptotic protection."
03/01/2009 - "The protective effects of nitric oxide (NO), a physiological activator of soluble guanylyl cyclase (sGC), have been reported in ischemia-reperfusion (I/R) syndrome of the lung. "
03/01/2009 - "Novel soluble guanylyl cyclase stimulator BAY 41-2272 attenuates ischemia-reperfusion-induced lung injury."
01/01/2013 - "In addition to activating soluble guanylyl cyclase (sGC)/cyclic guanosine monophosphate (cGMP)/protein kinase G (PKG) signaling pathways, NO-mediated protein S-nitros(yl)ation (SNO) has been recently shown to play an essential role in cardioprotection against ischemia-reperfusion (I/R) injury. "
05/15/2012 - "The hepatic soluble guanylyl cyclase-cyclic guanosine monophosphate pathway mediates the protection of remote ischemic preconditioning on the microcirculation in liver ischemia-reperfusion injury."
03/01/2013 - "We tested whether protection against reperfusion injury by ischemic postconditioning (IPost), soluble guanylyl cyclase (sGC) activation and inhibition, adenosine A(2B) receptor (A(2B)AR) agonist, phosphodiesterase type-5 (PDE-5) inhibitor, or mitochondria-targeted S-nitrosothiol (MitoSNO) was affected by a cardiomyocyte-specific ablation of the PKGI gene in the mouse (CMG-KO). "
|4.||Overactive Urinary Bladder (Overactive Bladder)
02/01/2014 - "We evaluated the effects of the soluble guanylyl cyclase activator BAY 60-2270 on voiding dysfunction and detrusor overactivity in a mouse model of obesity associated overactive bladder. "
02/01/2014 - "Activators of soluble guanylyl cyclase are of potential interest as treatment for cardiovascular diseases but to our knowledge they have never been proposed to treat overactive bladder. "
02/01/2014 - "The soluble guanylyl cyclase activator BAY 60-2770 ameliorates overactive bladder in obese mice."
09/01/2000 - "The aim of our present study as to evaluate the influence of atherosclerosis on the soluble guanylyl cyclase pathway in viable cultured smooth muscle cells (SMC) from rabbit atherosclerotic rabbit aortas (atherosclerotic SMC) and from control rabbit aortas (control SMC). "
04/01/2014 - "Activation of soluble guanylyl cyclase prevents foam cell formation and atherosclerosis."
01/15/1992 - "Since the lysolecithin content of LDLox correlated with the amount of lysolecithin necessary to diminish stimulation of soluble guanylyl cyclase, our data support the hypothesis that lysolecithin may be responsible for the inhibitory effect of LDLox on smooth muscle relaxation and provide evidence that the antagonistic effect of HDL against desensitization of soluble guanylyl cyclase by atherogenic compounds could be responsible for the protective role of HDL in atherosclerosis."
04/01/2015 - "In this review, we aim to place the genomic findings on components of the NO/cGMP pathway, namely endothelial nitric oxide synthase, soluble guanylyl cyclase and phosphodiesterase 5A, in context of preventive and therapeutic strategies for treating atherosclerosis and its sequelae. "
11/23/2004 - "Here, we show in the aortas of chronically hypercholesterolemic rabbits (a model of late-stage atherosclerosis), both subunits and specific activity of the NO receptor soluble guanylyl cyclase (sGC) were significantly reduced, whereas overall NO synthase activity was unaffected. "
|1.||Nitric Oxide (Nitrogen Monoxide)
|2.||Ascorbic Acid (Vitamin C)
|3.||4-(((4-carboxybutyl) (2- (5-fluoro-2-((4'-(trifluoromethyl) biphenyl-4-yl)methoxy)phenyl)ethyl) amino)methyl)benzoic acid
|4.||Adenosine A2B Receptor
|6.||Cyclic GMP-Dependent Protein Kinases (Protein Kinase G)
|8.||Peroxynitrous Acid (Peroxynitrite)
|10.||4- ethoxymethylene- 2- phenyl- 2- oxazoline- 5- one (phOx)