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

被引：106
|
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：
071010 ; 081704 ;
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
收藏
页码：2351 / 2355
页数：5
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