Chronic inhibition of cyclic GMP phosphodiesterase 5A prevents and reverses cardiac hypertrophy
暂无分享,去创建一个
D. Kass | Yibin Wang | E. Takimoto | H. Champion | Shuxun Ren | K. Gabrielson | Manxiang Li | E. Rodriguez | D. Bedja | Diego Belardi | S. Ren | E. Rodriguez
[1] M. Zaccolo,et al. cGMP Catabolism by Phosphodiesterase 5A Regulates Cardiac Adrenergic Stimulation by NOS3-Dependent Mechanism , 2004, Circulation research.
[2] L. Silengo,et al. PI3Kγ Modulates the Cardiac Response to Chronic Pressure Overload by Distinct Kinase-Dependent and -Independent Effects , 2004, Cell.
[3] M. Crackower,et al. The role of phosphoinositide-3 kinase and PTEN in cardiovascular physiology and disease. , 2004, Journal of molecular and cellular cardiology.
[4] E. Olson,et al. Glycogen synthase kinase-3β mediates convergence of protection signaling to inhibit the mitochondrial permeability transition pore , 2004 .
[5] R. Liao,et al. Glycogen synthase kinase-3beta regulates growth, calcium homeostasis, and diastolic function in the heart. , 2004, Journal of Biological Chemistry.
[6] C. Baylis,et al. Increased activity of cGMP-specific phosphodiesterase (PDE5) contributes to resistance to atrial natriuretic peptide natriuresis in the pregnant rat. , 2004, Journal of the American Society of Nephrology : JASN.
[7] B. Raju,et al. Clinical efficacy of sildenafil in primary pulmonary hypertension: a randomized, placebo-controlled, double-blind, crossover study. , 2004, Journal of the American College of Cardiology.
[8] E. Olson,et al. Hypertrophy of the heart: a new therapeutic target? , 2004, Circulation.
[9] D. Kass,et al. Modulation of In Vivo Cardiac Function by Myocyte-Specific Nitric Oxide Synthase-3 , 2004, Circulation research.
[10] Jian Xu,et al. Calcineurin/NFAT Coupling Participates in Pathological, but not Physiological, Cardiac Hypertrophy , 2004, Circulation research.
[11] E. Olson,et al. Cardiac hypertrophy: the good, the bad, and the ugly. , 2003, Annual review of physiology.
[12] C. Deschepper,et al. Expression of Constitutively Active Guanylate Cyclase in Cardiomyocytes Inhibits the Hypertrophic Effects of Isoproterenol and Aortic Constriction on Mouse Hearts* , 2003, Journal of Biological Chemistry.
[13] R. Pilz,et al. This Review Is Part of a Thematic Series on Cyclic Gmp–generating Enzymes and Cyclic Gmp–dependent Signaling, Which Includes the following Articles: Regulation of Nitric Oxide–sensitive Guanylyl Cyclase Cyclic Gmp Phosphodiesterases and Regulation of Smooth Muscle Function Structure, Regulation, and , 2022 .
[14] J. Balligand,et al. Nitric Oxide and Cardiac Function: Ten Years After, and Continuing , 2003, Circulation research.
[15] J. Beavo,et al. Regulation of Nitric Oxide–Sensitive Guanylyl Cyclase Cyclic GMP Phosphodiesterases and Regulation of Smooth Muscle Function Structure, Regulation, and Function of Membrane Guanylyl Cyclase Receptors, With a Focus on GC-A Cyclic GMP–Dependent Protein Kinases and the Cardiovascular System: Insights F , 2003 .
[16] R. Kloner,et al. Therapeutic potential of phosphodiesterase 5 inhibition for cardiovascular disease. , 2003, Circulation.
[17] J. Kotera,et al. cGMP-dependent protein kinase protects cGMP from hydrolysis by phosphodiesterase-5. , 2003, The Biochemical journal.
[18] Michael D. Schneider,et al. Pressure-independent cardiac hypertrophy in mice with cardiomyocyte-restricted inactivation of the atrial natriuretic peptide receptor guanylyl cyclase-A. , 2003, The Journal of clinical investigation.
[19] A. Rosenzweig,et al. Akt and PI 3-Kinase Signaling in Cardiomyocyte Hypertrophy and Survival , 2003, Cell cycle.
[20] J. Beavo,et al. PDE5 is converted to an activated state upon cGMP binding to the GAF A domain , 2003, The EMBO journal.
[21] H. Duff,et al. Time-dependent systolic and diastolic function in mice overexpressing calcineurin. , 2003, American Journal of Physiology. Heart and Circulatory Physiology.
[22] J. Corbin,et al. Sildenafil citrate does not affect cardiac contractility in human or dog heart , 2003, Current medical research and opinion.
[23] Y. S. Kim,et al. Phosphorylation of glycogen synthase kinase-3β at serine-9 by phospholipase Cγ1 through protein kinase C in rat 3Y1 fibroblasts , 2002, Experimental & Molecular Medicine.
[24] J. Kotera,et al. Phosphorylation of Isolated Human Phosphodiesterase-5 Regulatory Domain Induces an Apparent Conformational Change and Increases cGMP Binding Affinity* , 2002, The Journal of Biological Chemistry.
[25] J. Molkentin,et al. Involvement of extracellular signal-regulated kinases 1/2 in cardiac hypertrophy and cell death. , 2002, Circulation research.
[26] N. Yorioka,et al. A-Kinase Anchoring Protein AKAP220 Binds to Glycogen Synthase Kinase-3β (GSK-3β) and Mediates Protein Kinase A-dependent Inhibition of GSK-3β* , 2002, The Journal of Biological Chemistry.
[27] C. Kahn,et al. Regulation of Myocardial Contractility and Cell Size by Distinct PI3K-PTEN Signaling Pathways , 2002, Cell.
[28] J. Ross,et al. Akt induces enhanced myocardial contractility and cell size in vivo in transgenic mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[29] H. Drexler,et al. Inhibition of calcineurin-NFAT hypertrophy signaling by cGMP-dependent protein kinase type I in cardiac myocytes , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[30] S. Cook,et al. Phenotypic Spectrum Caused by Transgenic Overexpression of Activated Akt in the Heart* , 2002, The Journal of Biological Chemistry.
[31] P. Manow. ‚The Good, the Bad, and the Ugly‘ , 2002 .
[32] J. Sadoshima,et al. Glycogen synthase kinase-3beta: a novel regulator of cardiac hypertrophy and development. , 2002, Circulation Research.
[33] J. Molkentin,et al. Impaired cardiac hypertrophic response in Calcineurin Aβ-deficient mice , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[34] Michael D. Schneider,et al. MEKK1 is essential for cardiac hypertrophy and dysfunction induced by Gq , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[35] E. Olson,et al. Activated glycogen synthase-3β suppresses cardiac hypertrophy in vivo , 2002, Proceedings of the National Academy of Sciences of the United States of America.
[36] C. Trautwein,et al. Gene Transfer of cGMP-Dependent Protein Kinase I Enhances the Antihypertrophic Effects of Nitric Oxide in Cardiomyocytes , 2002, Hypertension.
[37] W. Koch,et al. Genetic Alterations That Inhibit In Vivo Pressure-Overload Hypertrophy Prevent Cardiac Dysfunction Despite Increased Wall Stress , 2002, Circulation.
[38] J. Beavo,et al. Upregulation of Phosphodiesterase 1A1 Expression Is Associated With the Development of Nitrate Tolerance , 2001, Circulation.
[39] D. Kass,et al. Cardiac phosphodiesterase 5 (cGMP‐specific) modulates β‐adrenergic signaling in vivo and is down‐regulated in heart failure , 2001, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
[40] Y. Zou,et al. Isoproterenol Activates Extracellular Signal–Regulated Protein Kinases in Cardiomyocytes Through Calcineurin , 2001, Circulation.
[41] E. Marbán,et al. Mitochondrial ATP-Sensitive Potassium Channels Inhibit Apoptosis Induced by Oxidative Stress in Cardiac Cells , 2001, Circulation research.
[42] J. Knowles,et al. Pressure-independent enhancement of cardiac hypertrophy in natriuretic peptide receptor A-deficient mice. , 2001, The Journal of clinical investigation.
[43] D. Garbers,et al. A genetic model provides evidence that the receptor for atrial natriuretic peptide (guanylyl cyclase-A) inhibits cardiac ventricular myocyte hypertrophy , 2001, Proceedings of the National Academy of Sciences of the United States of America.
[44] J. Corbin,et al. Cyclic nucleotide phosphodiesterases: relating structure and function. , 2001, Progress in nucleic acid research and molecular biology.
[45] R. Kitsis,et al. The MEK1–ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice , 2000, The EMBO journal.
[46] J. Molkentin,et al. Calcineurin Promotes Protein Kinase C and c-Jun NH2-terminal Kinase Activation in the Heart , 2000, The Journal of Biological Chemistry.
[47] G. Condorelli,et al. Calcineurin-mediated hypertrophy protects cardiomyocytes from apoptosis in vitro and in vivo: An apoptosis-independent model of dilated heart failure. , 2000, Circulation research.
[48] I. Goldstein,et al. Oral sildenafil in the treatment of erectile dysfunction. Sildenafil Study Group. , 1998, The New England journal of medicine.
[49] P. Wright,et al. Pharmacokinetics and metabolism of sildenafil in mouse, rat, rabbit, dog and man. , 1999, Xenobiotica; the fate of foreign compounds in biological systems.
[50] Tom F. Lue,et al. Oral sildenafil in the treatment of erectile dysfunction. Sildenafil Study Group. , 1998, New England Journal of Medicine.
[51] Jeffrey Robbins,et al. A Calcineurin-Dependent Transcriptional Pathway for Cardiac Hypertrophy , 1998, Cell.
[52] H. S. Kim,et al. Hypertension, cardiac hypertrophy, and sudden death in mice lacking natriuretic peptide receptor A. , 1997, Proceedings of the National Academy of Sciences of the United States of America.