Soluble guanylate cyclase: a potential therapeutic target for heart failure
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P. Ponikowski | J. Cleland | M. Gheorghiade | M. Metra | J. Butler | B. Pitt | G. Fonarow | J. Stasch | A. Voors | Lothar Roessig | P. Levy | M. Böhm | S. Collins | N. Sato | H. Sabbah | J. Burnett | S. Greene | U. Campia | Catherine N. Marti | L. Roessig
[1] G. Filippatos,et al. Treatment of acute decompensated heart failure with the soluble guanylate cyclase activator cinaciguat: The COMPOSE program – three randomized, controlled, phase IIb studies , 2011 .
[2] J. Stasch,et al. Measuring oxidative burden and predicting pharmacological response in coronary artery disease patients with a novel direct activator of haem-free/oxidised sGC. , 2011, Atherosclerosis.
[3] J. Stasch,et al. Additional stimulation of sGC on top of standard treatment with ARB`s may offer a new therapeutic approach for the treatment of diabetic nephropathy resistant to ARB treatment alone , 2011, BMC Pharmacology.
[4] M. Gheorghiade,et al. Improving postdischarge outcomes in patients hospitalized for acute heart failure syndromes. , 2011, JAMA.
[5] Pál Pacher,et al. Soluble guanylate cyclase as an emerging therapeutic target in cardiopulmonary disease. , 2011, Circulation.
[6] T. Sugaya,et al. Urinary L-type fatty acid-binding protein as a new renal biomarker in critical care , 2010, Current opinion in critical care.
[7] T. Münzel,et al. Is oxidative stress a therapeutic target in cardiovascular disease? , 2010, European heart journal.
[8] J. Bauersachs,et al. Guanylyl cyclase activator ataciguat improves vascular function and reduces platelet activation in heart failure. , 2010, Pharmacological research.
[9] J. Stasch,et al. Nitric oxide-independent stimulation of soluble guanylate cyclase reduces organ damage in experimental low-renin and high-renin models , 2010, Journal of hypertension.
[10] J. Stasch,et al. Structure of Cinaciguat (BAY 58–2667) Bound to Nostoc H-NOX Domain Reveals Insights into Heme-mimetic Activation of the Soluble Guanylyl Cyclase* , 2010, The Journal of Biological Chemistry.
[11] D. Mozaffarian,et al. Heart disease and stroke statistics--2010 update: a report from the American Heart Association. , 2010, Circulation.
[12] R. Kitsis,et al. Cell death in the pathogenesis of heart disease: mechanisms and significance. , 2010, Annual review of physiology.
[13] J. Hansen,et al. Soluble Guanylate Cyclase Agonists Inhibit Expression and Procoagulant Activity of Tissue Factor , 2009, Arteriosclerosis, thrombosis, and vascular biology.
[14] J. Stasch,et al. Acute hemodynamic response to single oral doses of BAY 60-4552, a soluble guanylate cyclase stimulator, in patients with biventricular heart failure , 2009, BMC Pharmacology.
[15] J. Stasch,et al. Cardioprotective effects in aged spontaneously hypertensive rats due to chronic stimulation/activation of sGC without hypotension , 2009, BMC Pharmacology.
[16] J. Stasch,et al. NO-insensitive sGCbeta1 H105F knockin mice: if NO has no place to go , 2009, BMC Pharmacology.
[17] J. Stasch,et al. Pressure-independent effects of pharmacological stimulation of soluble guanylate cyclase on fibrosis in pressure-overloaded rat heart , 2009, Hypertension Research.
[18] HaraldLapp,et al. Cinaciguat (BAY 58–2667) Improves Cardiopulmonary Hemodynamics in Patients With Acute Decompensated Heart Failure , 2009 .
[19] I. Piña,et al. Phase III clinical trial end points in acute heart failure syndromes: a virtual roundtable with the Acute Heart Failure Syndromes International Working Group. , 2009, American heart journal.
[20] J. Stasch,et al. Discovery of Riociguat (BAY 63‐2521): A Potent, Oral Stimulator of Soluble Guanylate Cyclase for the Treatment of Pulmonary Hypertension , 2009, ChemMedChem.
[21] Rebecca A Betensky,et al. Urinary Biomarkers for Sensitive and Specific Detection of Acute Kidney Injury in Humans , 2008, Clinical and translational science.
[22] P. Vermeersch,et al. Gender-specific hypertension and responsiveness to nitric oxide in sGCalpha1 knockout mice. , 2008, Cardiovascular research.
[23] K. Amann,et al. Blood Pressure-Independent Effect of Long-Term Treatment with the Soluble Heme-Independent Guanylyl Cyclase Activator HMR1766 on Progression in a Model of Noninflammatory Chronic Renal Damage , 2007, Kidney and Blood Pressure Research.
[24] T. Münzel,et al. Targeting heme-oxidized soluble guanylate cyclase: solution for all cardiorenal problems in heart failure? , 2007, Hypertension.
[25] K. Swedberg,et al. Effects of oral tolvaptan in patients hospitalized for worsening heart failure: the EVEREST Outcome Trial. , 2007, JAMA.
[26] M. Gheorghiade,et al. Prognostic markers in heart failure—congestion, neurohormones, and the cardiorenal syndrome , 2007, Acute cardiac care.
[27] Nancy M Albert,et al. Systolic blood pressure at admission, clinical characteristics, and outcomes in patients hospitalized with acute heart failure. , 2006, JAMA.
[28] J. Stasch,et al. Soluble Guanylate Cyclase Stimulation on Cardiovascular Remodeling in Angiotensin II–Induced Hypertensive Rats , 2006, Hypertension.
[29] M. Gladwin. Deconstructing endothelial dysfunction: soluble guanylyl cyclase oxidation and the NO resistance syndrome. , 2006, The Journal of clinical investigation.
[30] O. V. Evgenov,et al. NO-independent stimulators and activators of soluble guanylate cyclase: discovery and therapeutic potential , 2006, Nature Reviews Drug Discovery.
[31] J. Stasch,et al. Targeting the heme-oxidized nitric oxide receptor for selective vasodilatation of diseased blood vessels. , 2006, The Journal of clinical investigation.
[32] J. Stasch,et al. NO‐independent activation of soluble guanylate cyclase prevents disease progression in rats with 5/6 nephrectomy , 2006, British journal of pharmacology.
[33] W. Linz,et al. Biochemistry and Pharmacology of Novel Anthranilic Acid Derivatives Activating Heme-Oxidized Soluble Guanylyl Cyclase , 2006, Molecular Pharmacology.
[34] Luigi Tavazzi,et al. Acute Heart Failure Syndromes: Current State and Framework for Future Research , 2005, Circulation.
[35] Rudolf Berger,et al. Flow-mediated vasodilation predicts outcome in patients with chronic heart failure: comparison with B-type natriuretic peptide. , 2005, Journal of the American College of Cardiology.
[36] H. Kawachi,et al. Stimulation of soluble guanylate cyclase slows progression in anti-thy1-induced chronic glomerulosclerosis. , 2005, Kidney international.
[37] C. Szabó,et al. Nitrosative stress and pharmacological modulation of heart failure. , 2005, Trends in pharmacological sciences.
[38] J. Stasch,et al. Stimulation of soluble guanylyl cyclase inhibits mesangial cell proliferation and matrix accumulation in experimental glomerulonephritis. , 2005, American journal of physiology. Renal physiology.
[39] Stuart D Katz,et al. Vascular Endothelial Dysfunction and Mortality Risk in Patients With Chronic Heart Failure , 2005, Circulation.
[40] J. Mair,et al. Chronic heart failure is associated with vascular remodeling of the brachial artery , 2005, European journal of heart failure.
[41] H. Neumayer,et al. Expression and activity of soluble guanylate cyclase in injury and repair of anti-thy1 glomerulonephritis. , 2004, Kidney International.
[42] U. Zabel,et al. Reduced cGMP signaling associated with neointimal proliferation and vascular dysfunction in late-stage atherosclerosis. , 2004, Proceedings of the National Academy of Sciences of the United States of America.
[43] J. Bronzwaer,et al. Nitric oxide's role in the heart: control of beating or breathing? , 2004, American journal of physiology. Heart and circulatory physiology.
[44] S. Moncada,et al. Antiinflammatory activity of soluble guanylate cyclase: cGMP-dependent down-regulation of P-selectin expression and leukocyte recruitment. , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[45] Massimo Chiariello,et al. Endothelial Dysfunction and Cardiovascular Risk Prediction in Peripheral Arterial Disease: Additive Value of Flow-Mediated Dilation to Ankle-Brachial Pressure Index , 2003, Circulation.
[46] A. Ignaszewski,et al. The prognostic importance of endothelial dysfunction and carotid atheroma burden in patients with coronary artery disease. , 2003, Journal of the American College of Cardiology.
[47] J. Balligand,et al. Nitric Oxide and Cardiac Function: Ten Years After, and Continuing , 2003, Circulation research.
[48] S. Higano,et al. Abnormal coronary microvascular endothelial function in humans with asymptomatic left ventricular dysfunction. , 2003, American heart journal.
[49] Steven P Jones,et al. Endothelial nitric oxide synthase overexpression attenuates congestive heart failure in mice , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[50] J. Stasch,et al. Cardiorenal and Humoral Properties of a Novel Direct Soluble Guanylate Cyclase Stimulator BAY 41-2272 in Experimental Congestive Heart Failure , 2003, Circulation.
[51] A. Quyyumi,et al. Prognostic Value of Coronary Vascular Endothelial Dysfunction , 2002, Circulation.
[52] J. Stasch,et al. Cardiovascular actions of a novel NO‐independent guanylyl cyclase stimulator, BAY 41‐8543: in vivo studies , 2002, British journal of pharmacology.
[53] J. Stasch,et al. Pharmacological actions of a novel NO‐independent guanylyl cyclase stimulator, BAY 41‐8543: in vitro studies , 2002, British journal of pharmacology.
[54] M. Pfeffer,et al. Pulsatile Hemodynamics in Congestive Heart Failure , 2001, Hypertension.
[55] M. Mulvany,et al. Influence of Nitric Oxide Synthase and Adrenergic Inhibition on Adenosine-Induced Myocardial Hyperemia , 2001, Circulation.
[56] Richard T. Lee,et al. Endothelial Nitric Oxide Synthase Limits Left Ventricular Remodeling After Myocardial Infarction in Mice , 2001, Circulation.
[57] J. Stasch,et al. NO-independent stimulators of soluble guanylate cyclase. , 2001, Bioorganic & medicinal chemistry letters.
[58] R. Gerzer,et al. NO-independent regulatory site on soluble guanylate cyclase , 2001, Nature.
[59] W. Colucci,et al. Secondary pulmonary hypertension in chronic heart failure: the role of the endothelium in pathophysiology and management. , 2000, Circulation.
[60] T. Bachetti. Endothelial dysfunction in chronic heart failure: some new basic mechanisms. , 2000, Italian heart journal : official journal of the Italian Federation of Cardiology.
[61] F. Lallemand,et al. Improvement of endothelial function by chronic angiotensin-converting enzyme inhibition in heart failure : role of nitric oxide, prostanoids, oxidant stress, and bradykinin. , 2000, Circulation.
[62] J. Michel,et al. Hemodynamic stresses induce endothelial dysfunction and remodeling of pulmonary artery in experimental compensated heart failure. , 2000, Circulation.
[63] A M Zeiher,et al. Prognostic impact of coronary vasodilator dysfunction on adverse long-term outcome of coronary heart disease. , 2000, Circulation.
[64] S. Higano,et al. Long-term follow-up of patients with mild coronary artery disease and endothelial dysfunction. , 2000, Circulation.
[65] Paul C. Lee,et al. Endothelial dysfunction in patients with heart failure: relationship to disease severity. , 2000, Journal of cardiac failure.
[66] R. Ferrari,et al. Serum from patients with severe heart failure downregulates eNOS and is proapoptotic: role of tumor necrosis factor-alpha. , 1999, Circulation.
[67] Y. Takahashi,et al. Effects of troglitazone on frequency of coronary vasospastic-induced angina pectoris in patients with diabetes mellitus. , 1999, The American journal of cardiology.
[68] J P Cooke,et al. Limb blood flow during exercise is dependent on nitric oxide. , 1998, Circulation.
[69] I. Palacios,et al. Coronary endothelial dysfunction in patients with acute-onset idiopathic dilated cardiomyopathy. , 1998, Journal of the American College of Cardiology.
[70] B. Lorell,et al. Effects of the nitric oxide donor sodium nitroprusside on intracellular pH and contraction in hypertrophied myocytes. , 1997, Circulation.
[71] C A Beltrami,et al. Apoptosis in the failing human heart. , 1997, The New England journal of medicine.
[72] B. Bozkurt,et al. Basic mechanisms in heart failure: the cytokine hypothesis. , 1996, Journal of cardiac failure.
[73] W. Paulus,et al. Myocardial contractile response to nitric oxide and cGMP. , 1996, Circulation.
[74] C. Jones,et al. Endothelial control of arterial distensibility is impaired in chronic heart failure. , 1995, Circulation.
[75] A. Zeiher,et al. Impaired endothelium-dependent vasodilation of coronary resistance vessels is associated with exercise-induced myocardial ischemia. , 1995, Circulation.
[76] W. Paulus,et al. Acute effects of nitric oxide on left ventricular relaxation and diastolic distensibility in humans. Assessment by bicoronary sodium nitroprusside infusion. , 1994, Circulation.
[77] E. Lakatta,et al. 8-bromo-cGMP reduces the myofilament response to Ca2+ in intact cardiac myocytes. , 1994, Circulation research.
[78] B. Greenberg,et al. Diminished endothelium-derived relaxing factor activity in an experimental model of chronic heart failure. , 1991, Circulation research.
[79] R D Fish,et al. Endothelium-dependent dilation of the coronary microvasculature is impaired in dilated cardiomyopathy. , 1990, Circulation.
[80] Seymour Reichlin,et al. Handbook of experimental pharmacology , 1984 .
[81] C. O'connor,et al. Factors associated with improvement in ejection fraction in clinical practice among patients with heart failure: findings from IMPROVE HF. , 2012, American heart journal.
[82] J. Stasch,et al. Soluble Guanylate Cyclase: Allosteric Activation and Redox Regulation , 2010 .
[83] J. Stasch,et al. NO-independent, haem-dependent soluble guanylate cyclase stimulators. , 2009, Handbook of experimental pharmacology.
[84] J. Stasch,et al. Handbook of Experimental Pharmacology 191. cGMP: generators, effectors and therapeutic implications. Preface. , 2009, Handbook of experimental pharmacology.
[85] J. Stasch,et al. cGMP: Generators, Effectors and Therapeutic Implications , 2009 .
[86] H. Kawachi,et al. Enhancing cGMP in experimental progressive renal fibrosis: soluble guanylate cyclase stimulation vs. phosphodiesterase inhibition. , 2006, American journal of physiology. Renal physiology.
[87] H. Drexler,et al. Endothelial dysfunction in patients with chronic heart failure is independently associated with increased incidence of hospitalization, cardiac transplantation, or death. , 2005, European heart journal.
[88] N. Vaziri,et al. A high-fat, refined-carbohydrate diet induces endothelial dysfunction and oxidant/antioxidant imbalance and depresses NOS protein expression. , 2005, Journal of applied physiology.
[89] G. Schuler,et al. Exercise Capacity in Patients With Chronic Heart Failure Regular Physical Exercise Corrects Endothelial Dysfunction and Improves , 1998 .
[90] P. Vanhoutte. Endothelial dysfunction and vascular disease. , 1998, Verhandelingen - Koninklijke Academie voor Geneeskunde van Belgie.
[91] G. Kojda,et al. Low increase in cGMP induced by organic nitrates and nitrovasodilators improves contractile response of rat ventricular myocytes. , 1996, Circulation research.