Protein kinase cascades in the regulation of cardiac hypertrophy

被引:508
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
  • [31] Differential regulation of mitogen-activated protein kinases in the failing human heart in response to mechanical unloading
    Flesch, M
    Margulies, KB
    Mochmann, HC
    Engel, D
    Sivasubramanian, N
    Mann, DL
    [J]. CIRCULATION, 2001, 104 (19) : 2273 - 2276
  • [32] Preservation of base-line hemodynamic function and loss of inducible cardioprotection in adult mice lacking protein kinase Cε
    Gray, MO
    Zhou, HZ
    Schafhalter-Zoppoth, I
    Zhu, PL
    Mochly-Rosen, D
    Messing, RO
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (05) : 3596 - 3604
  • [33] WALL STRESS AND PATTERNS OF HYPERTROPHY IN HUMAN LEFT-VENTRICLE
    GROSSMAN, W
    JONES, D
    MCLAURIN, LP
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1975, 56 (01) : 56 - 64
  • [34] INCREASED PROTEIN-KINASE-C AND ISOZYME REDISTRIBUTION IN PRESSURE-OVERLOAD CARDIAC-HYPERTROPHY IN THE RAT
    GU, X
    BISHOP, SP
    [J]. CIRCULATION RESEARCH, 1994, 75 (05) : 926 - 931
  • [35] Protein kinase Cα negatively regulates systolic and diastolic function in pathological hypertrophy
    Hahn, HS
    Marreez, Y
    Odley, A
    Sterbling, A
    Yussman, MG
    Hilty, KC
    Bodi, I
    Liggett, SB
    Schwartz, A
    Dorn, GW
    [J]. CIRCULATION RESEARCH, 2003, 93 (11) : 1111 - 1119
  • [36] Ischemic protection and myofibrillar cardiomyopathy -: Dose-dependent effects of in vivo δPKC inhibition
    Hahn, HS
    Yussman, MG
    Toyokawa, T
    Marreez, Y
    Barrett, TJ
    Hilty, KC
    Osinska, H
    Robbins, J
    Dorn, GW
    [J]. CIRCULATION RESEARCH, 2002, 91 (08) : 741 - 748
  • [37] Stabilization of β-catenin by a Wnt-independent mechanism regulates cardiomyocyte growth
    Haq, S
    Michael, A
    Andreucci, M
    Bhattacharya, K
    Dotto, P
    Walters, B
    Woodgett, J
    Kilter, H
    Force, T
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (08) : 4610 - 4615
  • [38] Glycogen synthase kinase-3β is a negative regulator of cardiomyocyte hypertrophy
    Haq, S
    Choukroun, G
    Kang, ZB
    Ranu, H
    Matsui, T
    Rosenzweig, A
    Molkentin, JD
    Alessandrini, A
    Woodgett, J
    Hajjar, R
    Michael, A
    Force, T
    [J]. JOURNAL OF CELL BIOLOGY, 2000, 151 (01) : 117 - 129
  • [39] Haq S, 2001, CIRCULATION, V103, P670
  • [40] Phosphorylation of eukaryotic translation initiation factor 2Bε by glycogen synthase kinase-3β regulates β-adrenergic cardiac myocyte hypertrophy
    Hardt, SE
    Tomita, H
    Katus, HA
    Sadoshima, J
    [J]. CIRCULATION RESEARCH, 2004, 94 (07) : 926 - 935