Glycogen synthase kinase-3β -: A novel regulator of cardiac hypertrophy and development

被引:336
作者
Hardt, SE
Sadoshima, J
机构
[1] Univ Med & Dent New Jersey, New Jersey Med Sch, Inst Cardiovasc Res, Dept Cell Biol & Mol Med, Newark, NJ 07103 USA
[2] Univ Med & Dent New Jersey, New Jersey Med Sch, Inst Cardiovasc Res, Dept Med, Newark, NJ 07103 USA
关键词
glycogen synthase kinase-3 beta; hypertrophy; development; Akt; Wnt pathway;
D O I
10.1161/01.RES.0000018952.70505.F1
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Glycogen synthase kinase-3beta (GSK-3beta) is a ubiquitously expressed constitutively active serine/threonine kinase that phosphorylates cellular substrates and thereby regulates a wide variety of cellular functions, including development, metabolism, gene transcription, protein translation, cytoskeletal organization, cell cycle regulation, and apoptosis. The activity of GSK-3beta is negatively regulated by protein kinase B/Akt and by the Wnt signaling pathway. Increasing lines of evidence show that GSK-3beta is an essential negative regulator of cardiac hypertrophy and that the inhibition of GSK-3beta by hypertrophic stimuli is an important mechanism contributing to the development of cardiac hypertrophy. GSK-3beta also plays an important role in regulating cardiac development. In this review. the role of GSK-3beta in cardiac hypertrophy and development and the potential underlying mechanisms are discussed.
引用
收藏
页码:1055 / 1063
页数:9
相关论文
共 139 条
[1]   beta-catenin is a target for the ubiquitin-proteasome pathway [J].
Aberle, H ;
Bauer, A ;
Stappert, J ;
Kispert, A ;
Kemler, R .
EMBO JOURNAL, 1997, 16 (13) :3797-3804
[2]   Cyclin A/cdk2 activation is involved in hypoxia-induced apoptosis in cardiomyocytes [J].
Adachi, S ;
Ito, H ;
Tamamori-Adachi, M ;
Ono, Y ;
Nozato, T ;
Abe, S ;
Ikeda, M ;
Marumo, F ;
Hiroe, M .
CIRCULATION RESEARCH, 2001, 88 (04) :408-414
[3]   Wnt-1 regulation of connexin43 in cardiac myocytes [J].
Ai, ZW ;
Fischer, A ;
Spray, DC ;
Brown, AMC ;
Fishman, GI .
JOURNAL OF CLINICAL INVESTIGATION, 2000, 105 (02) :161-171
[4]   Phosphorylation-dependent regulation of cyclin D1 nuclear export and cyclin D1-dependent cellular transformation [J].
Alt, JR ;
Cleveland, JL ;
Hannink, M ;
Diehl, JA .
GENES & DEVELOPMENT, 2000, 14 (24) :3102-3114
[5]   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
[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]   Dual regulation of glycogen synthase kinase-3β by the α1A-adrenergic receptor [J].
Ballou, LM ;
Tian, PY ;
Lin, HY ;
Jiang, YP ;
Lin, RZ .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (44) :40910-40916
[8]   Nuclear export of NF-ATc enhanced by glycogen synthase kinase-3 [J].
Beals, CR ;
Sheridan, CM ;
Turck, CW ;
Gardner, P ;
Crabtree, GR .
SCIENCE, 1997, 275 (5308) :1930-1933
[9]   Functional interaction of an axin homolog, conductin, with β-catenin, APC, and GSK3β [J].
Behrens, J ;
Jerchow, BA ;
Würtele, M ;
Grimm, J ;
Asbrand, C ;
Wirtz, R ;
Kühl, M ;
Wedlich, D ;
Birchmeier, W .
SCIENCE, 1998, 280 (5363) :596-599
[10]   Proapoptotic stimuli induce nuclear accumulation of glycogen synthase kinase-3β [J].
Bijur, GN ;
Jope, RS .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (40) :37436-37442