Regulation of MEF2 by p38 MAPK and its implication in cardiomyocyte biology

被引：104

作者：

Han, JH ^{[1
]}

Molkentin, JD

机构：

[1] Scripps Res Inst, Dept Immunol, La Jolla, CA 92037 USA

[2] Childrens Hosp, Med Ctr, Div Mol Cardiovasc Biol, Cincinnati, OH 45229 USA

来源：

TRENDS IN CARDIOVASCULAR MEDICINE | 2000年 / 10卷 / 01期

关键词：

D O I：

10.1016/S1050-1738(00)00039-6

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Myocyte enhancer factor-2 (MEF2), transcription factors and mitogen-activated protein kinase (MAPK) p38 are regulators of cardiac development and various pathophysiologic processes. The recent finding that p38 can directly regulate MEF2 transcription factors suggests a novel mechanism for reprogramming cardiac gene expression in response to neuroendocrine and/or stress stimulation. This review weighs the accumulating evidence for a p38 MAPK-MEF2 signal transduction cascade and discusses ifs role in cardiac myocyte biology. (Trends Cardiovasc Med 2000; 10:19-22). (C) 2000 Elsevier Science Inc.

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页码：19 / 22

页数：4

相关论文

共 42 条

[1] Alterations in calcium handling in cardiac hypertrophy and heart failure [J].

Balke, CW ;

Shorofsky, SR .

CARDIOVASCULAR RESEARCH, 1998, 37 (02) :290-299

[2] Stimulation of the stress-activated mitogen-activated protein kinase subfamilies in perfused heart - p38/RK mitogen-activated protein kinases and c-Jun N-terminal kinases are activated by ischemia/reperfusion [J].

Bogoyevitch, MA ;

GillespieBrown, J ;

Ketterman, AJ ;

Fuller, SJ ;

BenLevy, R ;

Ashworth, A ;

Marshall, CJ ;

Sugden, PH .

CIRCULATION RESEARCH, 1996, 79 (02) :162-173

[3] Role of the stress-activated protein kinases in endothelin-induced cardiomyocyte hypertrophy [J].

Choukroun, G ;

Hajjar, R ;

Kyriakis, JM ;

Bonventre, JV ;

Rosenzweig, A ;

Force, T .

JOURNAL OF CLINICAL INVESTIGATION, 1998, 102 (07) :1311-1320

[4] 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? [J].

Clerk, A ;

Michael, A ;

Sugden, PH .

JOURNAL OF CELL BIOLOGY, 1998, 142 (02) :523-535

[5] Activation of c-Jun N-terminal kinases and p38-mitogen-activated protein kinases in human heart failure secondary to ischaemic heart disease [J].

Cook, SA ;

Sugden, PH ;

Clerk, A .

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1999, 31 (08) :1429-1434

[6] Stress-activated protein kinase-2 p38 and a rapamycin-sensitive pathway are required for C2C12 myogenesis [J].

Cuenda, A ;

Cohen, P .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (07) :4341-4346

[7]

Force T, 1999, GENE EXPRESSION, V7, P337

[8] Activation of the transcription factor MEF2C by the MAP kinase p38 in inflammation [J].

Han, J ;

Jiang, Y ;

Li, Z ;

Kravchenko, VV ;

Ulevitch, RJ .

NATURE, 1997, 386 (6622) :296-299

[9]

HAN TH, 1995, MOL CELL BIOL, V15, P2907

[10] Cell density and contraction regulate p38 MAP kinase-dependent responses in neonatal rat cardiac myocytes [J].

Hines, WA ;

Thorburn, J ;

Thorburn, A .

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1999, 277 (01) :H331-H341

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