Protein kinase cascades in the regulation of cardiac hypertrophy

被引:512
作者
Dorn, GW
Force, T
机构
[1] Univ Cincinnati, Med Ctr, Heart & Vasc Ctr, Cincinnati, OH 45267 USA
[2] Tufts Univ New England Med Ctr, Mol Cardiol Res Inst, Boston, MA USA
[3] Tufts Univ, Sch Med, Boston, MA 02111 USA
关键词
D O I
10.1172/JCI200524178
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
In broad terms, there are 3 types of cardiac hypertrophy: normal growth, growth induced by physical conditioning (i.e., physiologic hypertrophy), and growth induced by pathologic stimuli. Recent evidence suggests that normal and exercise-induced cardiac growth are regulated in large part by the growth hormone/IGF axis via signaling through the PI3K/Akt pathway. In contrast, pathological or reactive cardiac growth is triggered by autocrine and paracrine neurohormonal factors released during biomechanical stress that signal through the Gq/phospholipase C pathway, leading to an increase in cytosolic calcium and activation of PKC. Here we review recent developments in the area of these cardiotrophic kinases, highlighting the utility of animal models that are helping to identify molecular targets in the human condition.
引用
收藏
页码:527 / 537
页数:11
相关论文
共 109 条
[1]   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
[2]   Targeting the receptor-Gq interface to inhibit in vivo pressure overload myocardial hypertrophy [J].
Akhter, SA ;
Luttrell, LM ;
Rockman, HA ;
Iaccarino, G ;
Lefkowitz, RJ ;
Koch, WJ .
SCIENCE, 1998, 280 (5363) :574-577
[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]   Dynamic regulation of MEK/Erks and Akt/GSK-3β in human end-stage heart failure after left ventricular mechanical support:: myocardial mechanotransduction-sensitivity as a possible molecular mechanism [J].
Baba, HA ;
Stypmann, J ;
Grabellus, F ;
Kirchhof, P ;
Sokoll, A ;
Schäfers, M ;
Takeda, A ;
Wilhelm, MJ ;
Scheld, HH ;
Takeda, N ;
Breithardt, G ;
Levkau, B .
CARDIOVASCULAR RESEARCH, 2003, 59 (02) :390-399
[5]   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
[6]   Proliferative defect and embryonic lethality in mice homozygous for a deletion in the p110α subunit of phosphoinositide 3-kinase [J].
Bi, L ;
Okabe, I ;
Bernard, DJ ;
Wynshaw-Boris, A ;
Nussbaum, RL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (16) :10963-10968
[7]   Increased protein kinase C activity and expression of Ca2+-sensitive isoforms in the failing human heart [J].
Bowling, N ;
Walsh, RA ;
Song, GJ ;
Estridge, T ;
Sandusky, GE ;
Fouts, RL ;
Mintze, K ;
Pickard, T ;
Roden, R ;
Bristow, MR ;
Sabbah, HN ;
Mizrahi, JL ;
Gromo, G ;
King, GL ;
Vlahos, CJ .
CIRCULATION, 1999, 99 (03) :384-391
[8]   Expression of protein kinase C beta in the heart causes hypertrophy in adult mice and sudden death in neonates [J].
Bowman, JC ;
Steinberg, SF ;
Jiang, TR ;
Geenen, DL ;
Fishman, GI ;
Buttrick, PM .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 100 (09) :2189-2195
[9]   PKC-α regulates cardiac contractility and propensity toward heart failure [J].
Braz, JC ;
Gregory, K ;
Pathak, A ;
Zhao, W ;
Sahin, B ;
Klevitsky, R ;
Kimball, TF ;
Lorenz, JN ;
Nairn, AC ;
Liggett, SB ;
Bodi, I ;
Wang, S ;
Schwartz, A ;
Lakatta, EG ;
DePaoli-Roach, AA ;
Robbins, J ;
Hewett, TE ;
Bibb, JA ;
Westfall, MV ;
Kranias, EG ;
Molkentin, JD .
NATURE MEDICINE, 2004, 10 (03) :248-254
[10]   PKCα regulates the hypertrophic growth of cardiomyocytes through extracellular signal-regulated kinase1/2 (ERK1/2) [J].
Braz, JC ;
Bueno, OF ;
De Windt, LJ ;
Molkentin, JD .
JOURNAL OF CELL BIOLOGY, 2002, 156 (05) :905-919