Adaptive and maladaptive hypertrophic pathways: points of convergence and divergence

被引:128
作者
Selvetella, G
Hirsch, E
Notte, A
Tarone, G
Lembo, G
机构
[1] Univ Roma La Sapienza, IRCCS Neuromed, Dept Angiocardioneurol, Molise Sect, I-86077 Pozzilli, IS, Italy
[2] Univ Turin, Dept Genet Biol & Biochem, I-10126 Turin, Italy
[3] Univ Roma La Sapienza, Dept Expt Med & Pathol, Rome, Italy
关键词
left ventricular hypertrophy; signaling; transgenic mice; pressure overload;
D O I
10.1016/j.cardiores.2004.04.031
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Myocardial hypertrophy is a response of cardiac muscle to altered conditions of haemodynamic overload caused by a large number of physiological and pathological conditions. Traditionally, it has been considered a beneficial mechanism. However, sustained hypertrophy has been associated with a significant increase in the risk of cardiovascular disease and mortality. Actually, many researchers are trying to understand whether left ventricular hypertrophy is a 'good' mechanism to stimulate or a 'bad' process to prevent. In this review we investigate the most common biochemical signaling pathways involved in the hypertrophic response to identify the precise role, either 'adaptive' or 'maladaptive', of each molecular pathway. Delinealing intracellular signaling pathways involved in the different aspects of cardiac hypertrophy will permit future improvements in the signaling that controls beneficial growth. (C) 2004 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:373 / 380
页数:8
相关论文
共 96 条
[1]   G-proteins in growth and apoptosis: lessons from the heart [J].
Adams, JW ;
Brown, JH .
ONCOGENE, 2001, 20 (13) :1626-1634
[2]   Enhanced Gαq signaling:: A common pathway mediates cardiac hypertrophy and apoptotic heart failure [J].
Adams, JW ;
Sakata, Y ;
Davis, MG ;
Sah, VP ;
Wang, YB ;
Liggett, SB ;
Chien, KR ;
Brown, JH ;
Dorn, GW .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (17) :10140-10145
[3]   Activated glycogen synthase-3β suppresses cardiac hypertrophy in vivo [J].
Antos, CL ;
McKinsey, TA ;
Frey, N ;
Kutschke, W ;
McAnally, J ;
Shelton, JM ;
Richardson, JA ;
Hill, JA ;
Olson, EN .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2002, 99 (02) :907-912
[4]   Dilated cardiomyopathy and sudden death resulting from constitutive activation of protein kinase A [J].
Antos, CL ;
Frey, N ;
Marx, SO ;
Reiken, S ;
Gaburjakova, M ;
Richardson, JA ;
Marks, AR ;
Olson, EN .
CIRCULATION RESEARCH, 2001, 89 (11) :997-1004
[5]   β-Adrenergic receptor blockade arrests myocyte damage and preserves cardiac function in the transgenic Gsα mouse [J].
Asai, K ;
Yang, GP ;
Geng, YJ ;
Takagi, G ;
Bishop, S ;
Ishikawa, Y ;
Shannon, RP ;
Wagner, TE ;
Vatner, DE ;
Homcy, CJ ;
Vatner, SF .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 104 (05) :551-558
[6]   Fas receptor signaling inhibits glycogen synthase kinase 3β and induces cardiac hypertrophy following pressure overload [J].
Badorff, C ;
Ruetten, H ;
Mueller, S ;
Stahmer, M ;
Gehring, D ;
Jung, F ;
Ihling, C ;
Zeiher, AM ;
Dimmeler, S .
JOURNAL OF CLINICAL INVESTIGATION, 2002, 109 (03) :373-381
[7]   Hypertensive end-organ damage and premature mortality are p38 mitogen-activated protein kinase-dependent in a rat model of cardiac hypertrophy and dysfunction [J].
Behr, TM ;
Nerurkar, SS ;
Nelson, AH ;
Coatney, RW ;
Woods, TN ;
Sulpizio, A ;
Chandra, S ;
Brooks, DP ;
Kumar, S ;
Lee, JC ;
Ohlstein, EH ;
Angermann, CE ;
Adams, JL ;
Sisko, J ;
Sackner-Bernstein, JD ;
Willette, RN .
CIRCULATION, 2001, 104 (11) :1292-1298
[8]   MYOCARDIAL GI-ALPHA-PROTEIN LEVELS IN PATIENTS WITH HYPERTENSIVE CARDIAC-HYPERTROPHY, ISCHEMIC-HEART-DISEASE AND CARDIOGENIC-SHOCK [J].
BOHM, M ;
KIRCHMAYR, R ;
ERDMANN, E .
CARDIOVASCULAR RESEARCH, 1995, 30 (04) :611-618
[9]   PROGNOSTIC VALUE OF LEFT-VENTRICULAR MASS IN UNCOMPLICATED ACUTE MYOCARDIAL-INFARCTION AND ONE-VESSEL CORONARY-ARTERY DISEASE [J].
BOLOGNESE, L ;
DELLAVESA, P ;
ROSSI, L ;
SARASSO, G ;
BONGO, AS ;
SCIANARO, MC .
AMERICAN JOURNAL OF CARDIOLOGY, 1994, 73 (01) :1-5
[10]   Melusin is a new muscle-specific interactor for β1 integrin cytoplasmic domain [J].
Brancaccio, M ;
Guazzone, S ;
Menini, N ;
Sibona, E ;
Hirsch, E ;
De Andrea, M ;
Rocchi, M ;
Altruda, F ;
Tarone, G ;
Silengo, L .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (41) :29282-29288