Cardiac hypertrophy: sorting out the circuitry

被引:74
作者
McKinsey, TA [1 ]
Olson, EN [1 ]
机构
[1] Univ Texas, SW Med Ctr, Dept Mol Biol & Oncol, Dallas, TX 75235 USA
关键词
D O I
10.1016/S0959-437X(99)80040-9
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Cardiac hypertrophy is an adaptive response of the heart to a variety of intrinsic and extrinsic stimuli. The hypertrophic response, during which cardiomyocytes increase in size without undergoing cell division, initially serves to compensate for decreased cardiac output; however, prolonged hypertrophy can become detrimental, resulting in dilated cardiomyopathy and heart failure. Cardiac hypertrophy requires coupling of intracellular signal transduction systems with transcription factors that activate and maintain the hypertrophic program. Over the past year, signaling pathways involving G proteins, mitogen-activated protein kinases and calcium-responsive phosphatases have emerged as critical regulators of cardiac hypertrophy.
引用
收藏
页码:267 / 274
页数:8
相关论文
共 53 条
[21]   VENTRICULAR EXPRESSION OF A MLC-2V-RAS FUSION GENE INDUCES CARDIAC-HYPERTROPHY AND SELECTIVE DIASTOLIC DYSFUNCTION IN TRANSGENIC MICE [J].
HUNTER, JJ ;
TANAKA, N ;
ROCKMAN, HA ;
ROSS, J ;
CHIEN, KR .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (39) :23173-23178
[22]   CARDIAC-FUNCTION IN MICE OVEREXPRESSING THE BETA-ADRENERGIC-RECEPTOR KINASE OR A BETA-ARK INHIBITOR [J].
KOCH, WJ ;
ROCKMAN, HA ;
SAMAMA, P ;
HAMILTON, RA ;
BOND, RA ;
MILANO, CA ;
LEFKOWITZ, RJ .
SCIENCE, 1995, 268 (5215) :1350-1353
[23]  
Kodama H, 1997, CIRC RES, V81, P656
[24]   Calcineurin inhibitors and cardiac hypertrophy [J].
Luo, ZY ;
Shyu, KG ;
Gualberto, A ;
Walsh, K .
NATURE MEDICINE, 1998, 4 (10) :1092-1093
[25]   Cyclosporine attenuates pressure-overload hypertrophy in mice while enhancing susceptibility to decompensation and heart failure [J].
Meguro, T ;
Hong, C ;
Asai, K ;
Takagi, G ;
McKinsey, TA ;
Olson, EN ;
Vatner, SF .
CIRCULATION RESEARCH, 1999, 84 (06) :735-740
[26]   Transient cardiac expression of constitutively active Gαq leads to hypertrophy and dilated cardiomyopathy by calcineurin-dependent and independent pathways [J].
Mende, U ;
Kagen, A ;
Cohen, A ;
Aramburu, J ;
Schoen, FJ ;
Neer, EJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (23) :13893-13898
[27]   MYOCARDIAL EXPRESSION OF A CONSTITUTIVELY ACTIVE ALPHA(1B)-ADRENERGIC RECEPTOR IN TRANSGENIC MICE INDUCES CARDIAC-HYPERTROPHY [J].
MILANO, CA ;
DOLBER, PC ;
ROCKMAN, HA ;
BOND, RA ;
VENABLE, ME ;
ALLEN, LF ;
LEFKOWITZ, RJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (21) :10109-10113
[28]   Site-directed mutational analysis for the ATP binding of DnaA protein -: Functions of two conserved amino acids (Lys-178 and Asp-235) located in the ATP-binding domain of DnaA protein in vitro and in vivo [J].
Mizushima, T ;
Takaki, T ;
Kubota, T ;
Tsuchiya, T ;
Miki, T ;
Katayama, T ;
Sekimizu, K .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (33) :20847-20851
[29]  
Molkentin JD, 1997, CIRCULATION, V96, P3833
[30]   A calcineurin-dependent transcriptional pathway for cardiac hypertrophy [J].
Molkentin, JD ;
Lu, JR ;
Antos, CL ;
Markham, B ;
Richardson, J ;
Robbins, J ;
Grant, SR ;
Olson, EN .
CELL, 1998, 93 (02) :215-228