The p38 mitogen-activated protein kinase pathway-A potential target for intervention in infarction, hypertrophy, and heart failure

被引：138
作者：
Marber, Michael S. [1 ]
Rose, Beth [2 ,3 ,4 ]
Wang, Yibin [2 ,3 ,4 ]
机构：
[1] St Thomas Hosp, Rayne Inst, Div Cardiovasc, Kings Coll London,BHF Ctr,Rayne Inst, London SE1 7EH, England
[2] Univ Calif Los Angeles, Dept Anesthesiol, Los Angeles, CA 90095 USA
[3] Univ Calif Los Angeles, Dept Physiol, Los Angeles, CA 90095 USA
[4] Univ Calif Los Angeles, Dept Med, Los Angeles, CA 90095 USA
来源：
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY | 2011年 / 51卷 / 04期
关键词：
p38 kinase mitogen-activated protein kinase; Heart failure; Inhibitor; Therapy; P38-ALPHA MAP KINASE; SIGNAL-TRANSDUCTION; CONTRACTILE DYSFUNCTION; INDEPENDENT ACTIVATION; MYOCARDIAL-INFARCTION; SUSTAINED ISCHEMIA; TYROSINE KINASE; MOUSE MODEL; IN-VITRO; INHIBITION;
D O I：
10.1016/j.yjmcc.2010.10.021
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
The p38 mitogen-activated protein kinases (p38s) are stress-activated Ser/Thr kinases. Their activation has been associated with various pathological stressors in the heart. Activated p38 is implicated in a wide spectrum of cardiac pathologies, including hypertrophy, myocardial infarction, as well as systolic and diastolic heart failure. In this review, the specific contribution of different isoforms of p38 kinases to cardiac diseases as well as TAB-1-mediated non-canonical activation pathway are discussed as a rationale for inhibiting p38 activity to treat cardiac hypertrophy, ischemic injury, and heart failure. Finally, a summary of current clinical trials targeting p38 kinases in cardiovascular diseases is provided to highlight the potential promise as well as existing challenges of this therapeutic approach. This article is part of a special issue entitled "Key Signaling Molecules in Hypertrophy and Heart Failure." (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码：485 / 490
页数：6
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