Cardiac hypertrophy: Targeting Raf/MEK/ERK1/2-signaling

被引：145

作者：

Lorenz, Kristina ^{[1
]}

Schmitt, Joachim P. ^{[1
]}

Vidal, Marie ^{[1
]}

Lohse, Martin J. ^{[1
,2
]}

机构：

[1] Univ Wurzburg, Inst Pharmacol & Toxicol, D-97078 Wurzburg, Germany

[2] Univ Wurzburg, Rudolf Virchow Ctr, DFG Res Ctr Expt Biomed, D-97078 Wurzburg, Germany

来源：

INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY | 2009年 / 41卷 / 12期

关键词：

Cardiac hypertrophy; ERK1/2; Signaling; ACTIVATED PROTEIN-KINASE; EXTRACELLULAR SIGNAL; DIFFERENTIAL REGULATION; DILATED CARDIOMYOPATHY; INDUCED APOPTOSIS; HEART; INHIBITION; PATHWAY; DYSFUNCTION; MECHANISMS;

D O I：

10.1016/j.biocel.2009.08.002

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Over the past two decades, basic research has revealed a complex network of regulatory mechanisms that control the ERK1/2-signaling cascade. ERK1/2 mediate cardiac hypertrophy, a major risk factor for the development of arrhythmias, heart failure and sudden death, but also beneficial effects, e.g. protection of the heart from cell death and ischemic injury. Selective targeting of these ambiguous ERK functions could provide a powerful tool in the treatment of cardiac disease. This short review will discuss new mechanistic insights into ERK1/2-dependent development of cardiac hypertrophy and the prospect to translate this knowledge into future therapeutic strategies. (C) 2009 Elsevier Ltd. All rights reserved.

引用

页码：2351 / 2355

页数：5

共 32 条

[1]

The RAS/MAPK syndromes: Novel roles of the RAS pathway in human genetic disorders [J].

Aoki, Yoko ;

Niihori, Tetsuya ;

Narumi, Yoko ;

Kure, Shigeo ;

Matsubara, Yoichi .

HUMAN MUTATION, 2008, 29 (08) :992-1006

[2]

The MEK1-ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice [J].

Bueno, OF ;

De Windt, LJ ;

Tymitz, KM ;

Witt, SA ;

Kimball, TR ;

Klevitsky, R ;

Hewett, TE ;

Jones, SP ;

Lefer, DJ ;

Peng, CF ;

Kitsis, RN ;

Molkentin, JD .

EMBO JOURNAL, 2000, 19 (23) :6341-6350

[3]

Hypertrophic and dilated cardiomyopathy mutations differentially affect the molecular force generation of mouse α-cardiac myosin in the laser trap assay [J].

Debold, Edward P. ;

Schmitt, J. P. ;

Patlak, J. B. ;

Beck, S. E. ;

Moore, J. R. ;

Seidman, J. G. ;

Seidman, C. ;

Warshaw, D. M. .

AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2007, 293 (01) :H284-H291

[4]

Genetic alterations that inhibit in vivo pressure-overload hypertrophy prevent cardiac dysfunction despite increased wall stress [J].

Esposito, G ;

Rapacciuolo, A ;

Prasad, SVN ;

Takaoka, H ;

Thomas, SA ;

Koch, WJ ;

Rockman, HA .

CIRCULATION, 2002, 105 (01) :85-92

[5]

Hypertrophy of the heart - A new therapeutic target? [J].

Frey, N ;

Katus, HA ;

Olson, EN ;

Hill, JA .

CIRCULATION, 2004, 109 (13) :1580-1589

[6]

A New Gq-Initiated MAPK Signaling Pathway in the Heart [J].

Gutkind, J. Silvio ;

Offermanns, Stefan .

DEVELOPMENTAL CELL, 2009, 16 (02) :163-164

[7]

Raf-1 kinase is required for cardiac hypertrophy and cardiomyocyte survival in response to pressure overload [J].

Harris, IS ;

Zhang, SS ;

Treskov, I ;

Kovacs, A ;

Weinheimer, C ;

Muslin, AJ .

CIRCULATION, 2004, 110 (06) :718-723

[8]

Regulation of cardiac hypertrophy by intracellular signalling pathways [J].

Heineke, Joerg ;

Molkentin, Jeffery D. .

NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2006, 7 (08) :589-600

[9]

Mechanisms of disease: Cardiac plasticity [J].

Hill, Joseph A. ;

Olson, Eric N. .

NEW ENGLAND JOURNAL OF MEDICINE, 2008, 358 (13) :1370-1380

[10]

Hindley A, 2002, J CELL SCI, V115, P1575

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