In vivo effects of propyl gallate, a novel Ca(2+) sensitizer, in a mouse model of dilated cardiomyopathy caused by cardiac troponin T mutation.

[1]  R. Rose,et al.  Distinct Patterns of Constitutive Phosphodiesterase Activity in Mouse Sinoatrial Node and Atrial Myocardium , 2012, PloS one.

[2]  D. Nugteren,et al.  Non-enzymic conversion of all-cis 8 11 14-eicosatriencoic acid into prostaglandin E1. , 2010 .

[3]  A. Mebazaa,et al.  Levosimendan: from basic science to clinical practice , 2009, Heart Failure Reviews.

[4]  Ji Myoung Kim,et al.  PICOT is a critical regulator of cardiac hypertrophy and cardiomyocyte contractility. , 2008, Journal of molecular and cellular cardiology.

[5]  K. Hirata,et al.  Vitamin C restores the contractile response to dobutamine and improves myocardial efficiency in patients with heart failure after anterior myocardial infarction. , 2007, American heart journal.

[6]  Yuan-yuan Wang,et al.  Knock-In Mouse Model of Dilated Cardiomyopathy Caused by Troponin Mutation , 2007, Circulation research.

[7]  Ji Myoung Kim,et al.  PICOT Inhibits Cardiac Hypertrophy and Enhances Ventricular Function and Cardiomyocyte Contractility , 2006, Circulation research.

[8]  D. Kass,et al.  Mechanisms and Use of Calcium-Sensitizing Agents in the Failing Heart , 2006, Circulation.

[9]  K. Gauthaman,et al.  Protective effect of propyl gallate against myocardial oxidative stress‐induced injury in rat , 2005, The Journal of pharmacy and pharmacology.

[10]  H. Watkins,et al.  Severe disease expression of cardiac troponin C and T mutations in patients with idiopathic dilated cardiomyopathy. , 2004, Journal of the American College of Cardiology.

[11]  M. Endoh Mechanisms of action of novel cardiotonic agents. , 2002, Journal of cardiovascular pharmacology.

[12]  R. Hershberger,et al.  Cardiac troponin T lysine 210 deletion in a family with dilated cardiomyopathy. , 2002, Journal of cardiac failure.

[13]  D. Fatkin,et al.  Molecular mechanisms of inherited cardiomyopathies. , 2002, Physiological reviews.

[14]  F. Takahashi‐Yanaga,et al.  Ca2+-desensitizing effect of a deletion mutation ΔK210 in cardiac troponin T that causes familial dilated cardiomyopathy , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[15]  S. Solomon,et al.  Mutations in sarcomere protein genes as a cause of dilated cardiomyopathy. , 2001, The New England journal of medicine.

[16]  D. Sawyer,et al.  Antioxidants and myocardial contractility: illuminating the "Dark Side" of beta-adrenergic receptor activation? , 2001, Circulation.

[17]  M. Kamisago Mutations in Sarcomere Protein Genes as a Cause of Dilated Cardiomyopathy , 2000 .

[18]  D. DeMets,et al.  A Dose-Dependent Increase in Mortality with Vesnarinone among Patients with Severe Heart Failure , 1998 .

[19]  A. Kitabatake,et al.  Different regulation of myofilament Ca2+ sensitivity in beta-escin-skinned cardiac and vascular smooth muscles. , 1997, European journal of pharmacology.

[20]  J. Lubsen,et al.  Effect of pimobendan on exercise capacity in patients with heart failure: main results from the Pimobendan in Congestive Heart Failure (PICO) trial. , 1996, Heart.

[21]  V. Fuster,et al.  Idiopathic dilated cardiomyopathy. , 1994, The New England journal of medicine.

[22]  W. Remme,et al.  Hemodynamic, neurohumoral, and myocardial energetic effects of pimobendan, a novel calcium-sensitizing compound, in patients with mild to moderate heart failure. , 1994, Journal of cardiovascular pharmacology.

[23]  G. Hutchins,et al.  The causes of dilated cardiomyopathy: a clinicopathologic review of 673 consecutive patients. , 1994, Journal of the American College of Cardiology.

[24]  W. Abelmann,et al.  Prevalence and etiology of idiopathic dilated cardiomyopathy (summary of a National Heart, Lung, and Blood Institute workshop. , 1992, The American journal of cardiology.

[25]  R. Hajjar,et al.  Calcium-sensitizing inotropic agents in the treatment of heart failure: A critical view , 1991, Cardiovascular Drugs and Therapy.

[26]  D. DeMets,et al.  Effect of oral milrinone on mortality in severe chronic heart failure. The PROMISE Study Research Group. , 1991, The New England journal of medicine.

[27]  D. Crankshaw,et al.  Synergistic actions of nitrovasodilators and isoprenaline on rat aortic smooth muscle. , 1991, European journal of pharmacology.

[28]  C. Lugnier,et al.  Role of cyclic AMP- and cyclic GMP-phosphodiesterases in the control of cyclic nucleotide levels and smooth muscle tone in rat isolated aorta. A study with selective inhibitors. , 1987, Biochemical pharmacology.

[29]  C. Lugnier,et al.  Selective inhibition of cyclic nucleotide phosphodiesterases of human, bovine and rat aorta. , 1986, Biochemical pharmacology.

[30]  J. R. Blinks,et al.  Modification of myofibrillar responsiveness to Ca++ as an inotropic mechanism. , 1986, Circulation.

[31]  Katz Am Potential deleterious effects of inotropic agents in the therapy of chronic heart failure. , 1986 .

[32]  F. Takahashi‐Yanaga,et al.  Propyl gallate, a strong antioxidant, increases the Ca2+ sensitivity of cardiac myofilament. , 2009, Journal of pharmacological sciences.

[33]  S. Morimoto Sarcomeric proteins and inherited cardiomyopathies. , 2008, Cardiovascular research.

[34]  F. Takahashi‐Yanaga,et al.  SCH00013, a novel Ca(2+) sensitizer with positive inotropic and no chronotropic action in heart failure. , 2005, Journal of pharmacological sciences.

[35]  T. Imaizumi,et al.  Functional changes in troponin T by a splice donor site mutation that causes hypertrophic cardiomyopathy , 1999 .