Genetic enhancement of ventricular contractility protects against pressure-overload-induced cardiac dysfunction.
暂无分享,去创建一个
R. Graham | Xiao-Ming Gao | H. Kiriazis | Xiao-Jun Du | A. Finch | E. Hotchkin | Xinheng Feng | L. Fang | H. Chaulet
[1] P. Doevendans,et al. MEK1-ERK2 Signaling Pathway Protects Myocardium From Ischemic Injury In Vivo , 2004, Circulation.
[2] M. Hori,et al. Targeted deletion of apoptosis signal-regulating kinase 1 attenuates left ventricular remodeling , 2003, Proceedings of the National Academy of Sciences of the United States of America.
[3] E. Foster,et al. The α1A/C- and α1B-adrenergic receptors are required for physiological cardiac hypertrophy in the double-knockout mouse , 2003 .
[4] R. Graham,et al. Cardiac-targeted overexpression of the α1A-AR results in premature death: A potential model of electromechanical dissociation , 2003 .
[5] B. Kemp,et al. Impaired Cardiac Contractility Response to Hemodynamic Stress in S100A1-Deficient Mice , 2002, Molecular and Cellular Biology.
[6] B. Hoit,et al. Hypertrophy and functional alterations in hyperdynamic phospholamban-knockout mouse hearts under chronic aortic stenosis. , 2002, Cardiovascular research.
[7] W. Koch,et al. Genetic Alterations That Inhibit In Vivo Pressure-Overload Hypertrophy Prevent Cardiac Dysfunction Despite Increased Wall Stress , 2002, Circulation.
[8] W. Manning,et al. Transgenic Expression of Sarcoplasmic Reticulum Ca2+ ATPase Modifies the Transition From Hypertrophy to Early Heart Failure , 2001, Circulation research.
[9] R. Graham,et al. Targeted &agr;1A-Adrenergic Receptor Overexpression Induces Enhanced Cardiac Contractility but not Hypertrophy , 2001, Circulation research.
[10] R. Lefkowitz,et al. Regulation of myocardial βARK1 expression in catecholamine-induced cardiac hypertrophy in transgenic mice overexpressing α1B-adrenergic receptors , 2001 .
[11] M. Zuscik,et al. Hypotension, Autonomic Failure, and Cardiac Hypertrophy in Transgenic Mice Overexpressing the α1B-Adrenergic Receptor* , 2001, The Journal of Biological Chemistry.
[12] D. Sawyer,et al. MEK1/2-ERK1/2 mediates alpha1-adrenergic receptor-stimulated hypertrophy in adult rat ventricular myocytes. , 2001, Journal of molecular and cellular cardiology.
[13] K. Schlüter,et al. Beta-adrenoceptor stimulation attenuates the hypertrophic effect of alpha-adrenoceptor stimulation in adult rat ventricular cardiomyocytes. , 2001, Journal of the American College of Cardiology.
[14] R. Kitsis,et al. The MEK1–ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice , 2000, The EMBO journal.
[15] W. Koch,et al. Physiological Induction of a &bgr;-Adrenergic Receptor Kinase Inhibitor Transgene Preserves &bgr;-Adrenergic Responsiveness in Pressure-Overload Cardiac Hypertrophy , 2000, Circulation.
[16] A. Dart,et al. Preserved ventricular contractility in infarcted mouse heart overexpressing beta(2)-adrenergic receptors. , 2000, American journal of physiology. Heart and circulatory physiology.
[17] P. Simpson,et al. Autonomous and growth factor-induced hypertrophy in cultured neonatal mouse cardiac myocytes. Comparison with rat. , 2000, Circulation research.
[18] E. Woodcock,et al. Adverse effects of constitutively active alpha(1B)-adrenergic receptors after pressure overload in mouse hearts. , 2000, American journal of physiology. Heart and circulatory physiology.
[19] A. Sabri,et al. The alpha(1)-adrenoceptor subtype- and protein kinase C isoform-dependence of Norepinephrine's actions in cardiomyocytes. , 2000, Journal of molecular and cellular cardiology.
[20] B. Wilson,et al. Coupling Function of Endogenous α1- and β-Adrenergic Receptors in Mouse Cardiomyocytes , 2000 .
[21] A. Dart,et al. beta(2)-adrenergic receptor overexpression exacerbates development of heart failure after aortic stenosis. , 2000, Circulation.
[22] M. Michel,et al. Adrenergic and muscarinic receptors in the human heart. , 1999, Pharmacological reviews.
[23] G. Boivin,et al. Overexpression of α1B-adrenergic receptor induces left ventricular dysfunction in the absence of hypertrophy. , 1998, American journal of physiology. Heart and circulatory physiology.
[24] E. Woodcock,et al. Selective activation of alpha1A-adrenergic receptors in neonatal cardiac myocytes is sufficient to cause hypertrophy and differential regulation of alpha1-adrenergic receptor subtype mRNAs. , 1998, Journal of molecular and cellular cardiology.
[25] E. Kranias,et al. Transgenic Approaches to Define the Functional Role of Dual Site Phospholamban Phosphorylation* , 1998, The Journal of Biological Chemistry.
[26] D. Varma,et al. Role of Ca(2+)-independent PKC in alpha 1-adrenoceptor-mediated inotropic responses of neonatal rat hearts. , 1997, The American journal of physiology.
[27] M. Cho,et al. Transgenic Mice with Cardiac Overexpression of α1B-Adrenergic Receptors , 1997, The Journal of Biological Chemistry.
[28] H. Rockman,et al. Overexpression of the rat sarcoplasmic reticulum Ca2+ ATPase gene in the heart of transgenic mice accelerates calcium transients and cardiac relaxation. , 1997, The Journal of clinical investigation.
[29] K. Chien,et al. The MEKK-JNK Pathway Is Stimulated by α1-Adrenergic Receptor and Ras Activation and Is Associated with in Vitroand in Vivo Cardiac Hypertrophy* , 1997, The Journal of Biological Chemistry.
[30] J. Rouleau,et al. Myocardial alpha1-adrenoceptor: inotropic effect and physiologic and pathologic implications. , 1997, Life sciences.
[31] C. Long,et al. Alpha1-adrenergic receptor subtype mRNAs are differentially regulated by alpha1-adrenergic and other hypertrophic stimuli in cardiac myocytes in culture and in vivo. Repression of alpha1B and alpha1D but induction of alpha1C. , 1996, The Journal of biological chemistry.
[32] R. Lefkowitz,et al. Myocardial expression of a constitutively active alpha 1B-adrenergic receptor in transgenic mice induces cardiac hypertrophy. , 1994, Proceedings of the National Academy of Sciences of the United States of America.
[33] R. Kennedy,et al. WB4101- and CEC-sensitive positive inotropic actions of phenylephrine in rat cardiac muscle. , 1994, The American journal of physiology.
[34] R. Dilley,et al. Mineralocorticoids, hypertension, and cardiac fibrosis. , 1994, The Journal of clinical investigation.
[35] R. Lefkowitz,et al. Enhanced myocardial function in transgenic mice overexpressing the beta 2-adrenergic receptor. , 1994, Science.
[36] J. Ross,et al. Segregation of atrial-specific and inducible expression of an atrial natriuretic factor transgene in an in vivo murine model of cardiac hypertrophy , 1991, Proceedings of the National Academy of Sciences of the United States of America.
[37] K. Chien,et al. Erratum: Segregation of atrial-specific and inducible expression of an atrial natriuretic factor transgene in an in vivo murine model of cardiac hypertrophy (Proc. Natl. Acad. Sci. USA (September 1991) 88 (8277-8281)) , 1991 .
[38] V. Sukhatme,et al. Alpha- and beta-adrenergic stimulation induces distinct patterns of immediate early gene expression in neonatal rat myocardial cells. fos/jun expression is associated with sarcomere assembly; Egr-1 induction is primarily an alpha 1-mediated response. , 1990, The Journal of biological chemistry.
[39] P. Simpson. Norepinephrine-stimulated hypertrophy of cultured rat myocardial cells is an alpha 1 adrenergic response. , 1983, The Journal of clinical investigation.