mécanismes moléculaires de l'hypertrophie ventriculaire gauche
mécanismes moléculaires de l'hypertrophie ventriculaire gauche
mécanismes moléculaires de l'hypertrophie ventriculaire gauche
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MÉCANISMES MOLÉCULAIRES DE L’HYPERTROPHIE VENTRICULAIRE GAUCHE 23544. NEUMANN J, SCHMITZ W, SCHOLZ H et al. Increase in myocardial Gi-proteins in heart failure. Lancet,1988, 2, 936-937.45. BOHM M, GIERSCHIK P, KNORR A et al. Desensitization of a<strong>de</strong>nylate cyclase and increase of Gialpha in cardiac hypertrophy due to acquired hypertension. Hypertension, 1992, 20, 103-112.46. VATNER D, SATO N, GALPER J et al. Physiological and biochemical evi<strong>de</strong>nce for coordinateincreases in muscarinic receptors and Gi during pacing-induced heart failure. Circulation, 1996,94, 102-107.47. LAMORTE VJ, THORBURN J, ABSHER D et al. Gq- and ras-<strong>de</strong>pen<strong>de</strong>nt pathways mediate hypertrophyof neonatal rat ventricular myocytes following alpha 1-adrenergic stimulation. J Biol Chem, 1994,269, 13490-13496.48. MENDE U, KAGEN A, COHEN A et al. Transient cardiac expression of constitutively active Gαqleads to hypertrophy and dilated cardiomyopathy by calcineurin-<strong>de</strong>pen<strong>de</strong>nt and in<strong>de</strong>pen<strong>de</strong>ntpathways. Proc Natl Acad Sci USA, 1998, 95, 13893-13898.49. D’ANGELO D, SAKATA Y, LORENS JN et al. Transgenic Gαq overexpression induces cardiaccontractile failure in mice. Proc Natl Acad Sci USA, 1997, 94, 8121-8126.50. AKHTER SA, LUTTRELL LM, ROCKMAN HA et al. Targeting the receptor-Gq interface to inhibit invivo pressure overload myocardial hypertrophy. Science, 1998, 280, 574-577.51. MELLOR H, PARKER PJ. The extented protein kinase C superfamily. Biochem J, 1998, 332, 281-292.52. GU X, BISHOP S. Increased protein kinase C and isozyme redistribution in pressure-overload cardiachypertrophy in the rat. Cir Res, 1994, 75, 926-931.53. MOLKENTIN JD, DORN II GW2nd. Cytoplasmic signaling pathways that regulate cardiac hypertrophy.Annu Rev Physiol, 2001, 63, 391-426.54. ZOU Y, KOMURO I, YAMAZAKI T et al. Protein kinase C, but not tyrosine kinases or Ras, plays acritical role in Angiotensin II-induced activation of Raf-1 kinase and extracellular signal-regulatedprotein kinases in cardiac myocytes. J Biol Chem, 1996, 271, 33592-33597.55. FORCE T, POMBO CM, AVRUCH JA et al. Stress-activated protein kinases in cardiovascular disease.Circ Res, 1996, 78, 947-953.56. FORCE T, BONVENTRE JV. Growth factors and mitogen-activated protein kinases. Hypertension,1998, 31, 152-161.57. KYRIAKIS JM, AVRUCH J. Protein kinase casca<strong>de</strong>s activated by stress and inflammatory cytokines.BioEssays, 1996, 18, 567-577.58. KYRIAKIS JM, BANERJEE P, NIKOLAKAKI E et al. The stress-activated protein kinase subfamily ofc-Jun kinases. Nature, 1994, 369, 156-160.59. COHEN P. The search for physiological substrates of mitogen- and stress-activated protein kinasesin mammalian cells. Trends Cell Biol, 1997, 7, 353-361.60. SUGDEN PH, CLERK A. “Stress responsive” mitogen-activated protein kinases (C-jun N- terminalkinases and p38 mitogen-activated protein kinases) in the myocardium. Circ Res, 1998, 83, 345-352.61. CLERK A, BOGOYEVITCH MA, ANDERSON MB et al. Differential activation of protein kinase C isoformsby endothelin-1 and phenylephrine and subsequent stimulation of p42 and p44 mitogenactivatedprotein kinases in ventricular myocytes cultured from neonatal rat hearts. J Biol Chem,1994, 269, 32848-32857.62. BOGOYEVITCH MA, GILLESPIE BJ, KetTerman AJ et al. Stimulation of the stress-activated mitogenactivatedprotein kinase subfamilies in perfused heart. p38/RK mitogen-activated protein kinasesand c-Jun N-terminal kinases are activated by ischemia/reperfusion. Circ Res, 1996, 79, 162-173.63. GILLESPIE-BROWN J, FULLER SJ, BOGOYEVITCH MA et al. The mitogen-activated protein kinasekinase MEK1 stimulates a pattern of gene expression typical of the hypertrophic phenotype in ratventricular cardiomyocytes. J Biol Chem, 1995, 270, 28092-28096.64. THORBURN J, CARLSON M, MANSOUR SJ et al. Inhibition of a signaling pathway in cardiac musclecells by active mitogen-activated protein kinase kinase. Mol Biol Cell, 1995, 6, 1479-1490.65. THORBURN J, MCMAHON M, THORBURN A. Raf-1 kinase activity is necessary and sufficient forgene expression changes but not sufficient for cellular morphology changes associated with cardiacmyocyte hypertrophy. J Biol Chem, 1994, 269, 30580-30586.66. CHOUKROUN G, HAJJAR R, KYRIAKIS JM et al. Role of the stress-activated protein kinases in endothelin-inducedcardiomyocyte hypertrophy. J Clin Invest, 1998, 102, 1311-1320.