Genetic factors in cardiac hypertrophy

被引：18

作者：

Dorn, GW ^{[1
]}

Hahn, HS ^{[1
]}

机构：

[1] Univ Cincinnati, Med Ctr, Heart & Vasc Ctr, Cincinnati, OH 45267 USA

来源：

CARDIAC ENGINEERING: FROM GENES AND CELLS TO STRUCTURE AND FUNCTION | 2004年 / 1015卷

关键词：

heart failure; receptor signaling; myocardial hypertrophy;

D O I：

10.1196/annals.1302.019

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

Cardiac hypertrophy is an adaptive response to any cardiac insult or stress that increases hemodynamic load. Cardiac hypertrophy can exist in a state of compensation or progress to a decompensated state (i.e., heart failure) over time. It has been established through transgenic overexpression and gene ablation studies that multiple signaling pathways are involved in the induction of hypertrophy as well as its decompensation. This article reviews the role of Galphaq in the development of pressure overload hypertrophy and discusses the relationships between Galphaq and beta-adrenergic receptors, RGS proteins, and the proapoptotic factor, Nix/Bnip3L.

引用

页码：225 / 237

页数：13

共 82 条

[51]

Naruse K, 2000, CIRC RES, V86, P1104

[52] STUDIES AND PERSPECTIVES OF PROTEIN-KINASE-C [J].

NISHIZUKA, Y .

SCIENCE, 1986, 233 (4761) :305-312

[53] In vivo functions of heterotrimeric G-proteins:: studies in Gα-deficient mice [J].

Offermanns, S .

ONCOGENE, 2001, 20 (13) :1635-1642

[54] Defective platelet activation in G alpha(q)-deficient mice [J].

Offermanns, S ;

Toombs, CF ;

Hu, YH ;

Simon, MI .

NATURE, 1997, 389 (6647) :183-186

[55] Embryonic cardiomyocyte hypoplasia and craniofacial defects in Gαq/Gα11-mutant mice [J].

Offermanns, S ;

Zhao, LP ;

Gohla, A ;

Sarosi, I ;

Simon, MI ;

Wilkie, TM .

EMBO JOURNAL, 1998, 17 (15) :4304-4312

[56] Apoptosis in the failing human heart [J].

Olivetti, G ;

Abbi, R ;

Quaini, F ;

Kajstura, J ;

Cheng, W ;

Nitahara, JA ;

Quaini, E ;

DiLoreto, C ;

Beltrami, CA ;

Krajewski, S ;

Reed, JC ;

Anversa, P .

NEW ENGLAND JOURNAL OF MEDICINE, 1997, 336 (16) :1131-1141

[57]

Osler W., PRINCIPLES PRACTICE

[58] PKCε activation induces dichotomous cardiac phenotypes and modulates PKCε-RACK interactions and RACK expression [J].

Pass, JM ;

Zheng, YT ;

Wead, WB ;

Zhang, J ;

Li, RCX ;

Bolli, R ;

Ping, PP .

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2001, 280 (03) :H946-H955

[59] Myocardial beta-adrenergic receptor signaling in vivo: Insights from transgenic mice [J].

Rockman, HA ;

Koch, WJ ;

Milano, CA ;

Lefkowitz, RJ .

JOURNAL OF MOLECULAR MEDICINE-JMM, 1996, 74 (09) :489-495

[60] Expression of a β-adrenergic receptor kinase 1 inhibitor prevents the development of myocardial failure in gene-targeted mice [J].

Rockman, HA ;

Chien, KR ;

Choi, DJ ;

Iaccarino, G ;

Hunter, JJ ;

Ross, J ;

Lefkowitz, RJ ;

Koch, WJ .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (12) :7000-7005

← 1 2 3 4 5 6 7 8 9 →