Signalling via stress-activated mitogen-activated protein kinases in the cardiovascular system

被引:88
作者
Bogoyevitch, MA [1 ]
机构
[1] Univ Western Australia, Dept Biochem, Nedlands, WA 6907, Australia
基金
英国医学研究理事会;
关键词
cytokines; gene expression; growth factors; protein kinases; signal transduction;
D O I
10.1016/S0008-6363(99)00386-7
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
A number of physiological, pharmacological and pathological stimuli initiate cardiac hypertrophy. The intracellular signalling events activated by these stimuli are equally complex. Our ability to treat the hypertrophic and failing myocardium effectively will require clarification of which signalling events regulate growth, remodelling and failure. Much recent attention has focused on the regulation of the mitogen-activated protein kinase cascades (MAPKs), with the importance of these cascades in the development of cardiovascular diseases being extensively explored. These signalling pathways may provide one link from the diverse stress and pharmacological extracellular stimuli to the regulation of gene expression, contractile protein regulation and protein function. This review focuses on the recent progress made in the understanding of the regulation and function of MAPKs in the cardiovascular system, with particular emphasis being placed on the events in the cardiac ventricular myocyte. (C) 2000 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:826 / 842
页数:17
相关论文
共 151 条
  • [21] Stimulation of the p38 mitogen-activated protein kinase pathway in neonatal rat ventricular myocytes by the G protein-coupled receptor agonists, endothelin-1 and phenylephrine: A role in cardiac myocyte hypertrophy?
    Clerk, A
    Michael, A
    Sugden, PH
    [J]. JOURNAL OF CELL BIOLOGY, 1998, 142 (02) : 523 - 535
  • [22] Stimulation of "Stress-regulated" mitogen-activated protein kinases (stress-activated protein kinases c-Jun N-terminal kinases and p38-mitogen-activated protein kinases) in perfused rat hearts by oxidative and other stresses
    Clerk, A
    Fuller, SJ
    Michael, A
    Sugden, PH
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (13) : 7228 - 7234
  • [23] HOW MAP KINASES ARE REGULATED
    COBB, MH
    GOLDSMITH, EJ
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1995, 270 (25) : 14843 - 14846
  • [24] Stress-activated protein kinase-2 p38 and a rapamycin-sensitive pathway are required for C2C12 myogenesis
    Cuenda, A
    Cohen, P
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (07) : 4341 - 4346
  • [25] Mitogen- and stress-activated protein kinase-1 (MSK1) is directly activated by MAPK and SAPK2/p38, and may mediate activation of CREB
    Deak, M
    Clifton, AD
    Lucocq, JM
    Alessi, DR
    [J]. EMBO JOURNAL, 1998, 17 (15) : 4426 - 4441
  • [26] JNK1 - A PROTEIN-KINASE STIMULATED BY UV-LIGHT AND HA-RAS THAT BINDS AND PHOSPHORYLATES THE C-JUN ACTIVATION DOMAIN
    DERIJARD, B
    HIBI, M
    WU, IH
    BARRETT, T
    SU, B
    DENG, TL
    KARIN, M
    DAVIS, RJ
    [J]. CELL, 1994, 76 (06) : 1025 - 1037
  • [27] PHORBOL ESTERS INDUCE IMMEDIATE-EARLY GENES AND ACTIVATE CARDIAC GENE-TRANSCRIPTION IN NEONATAL RAT MYOCARDIAL-CELLS
    DUNNMON, PM
    IWAKI, K
    HENDERSON, SA
    SEN, A
    CHIEN, KR
    [J]. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1990, 22 (08) : 901 - 910
  • [28] Functions of c-jun in liver and heart development
    Eferl, R
    Sibilia, M
    Hilberg, F
    Fuchsbichler, A
    Kufferath, I
    Guertl, B
    Zenz, R
    Wagner, EF
    Zatloukal, K
    [J]. JOURNAL OF CELL BIOLOGY, 1999, 145 (05) : 1049 - 1061
  • [29] ERIKSON RL, 1991, J BIOL CHEM, V266, P6007
  • [30] Dilated cardiomyopathy in transgenic mice expressing a dominant-negative CREB transcription factor in the heart
    Fentzke, RC
    Korcarz, CE
    Lang, RM
    Lin, H
    Leiden, JM
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1998, 101 (11) : 2415 - 2426