Derepression of pathological cardiac genes by members of the CaM kinase superfamily

被引：93

作者：

McKinsey, Timothy A. ^{[1
]}

机构：

[1] Myogen Inc Gilead Colorado Inc, Westminster, CO 80021 USA

来源：

CARDIOVASCULAR RESEARCH | 2007年 / 73卷 / 04期

关键词：

transcription; signaling; CaM kinase; histone deacetylase; chromatin;

D O I：

10.1016/j.cardiores.2006.11.036

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

In response to pathologic stresses such as hypertension or myocardial infarction, the heart undergoes a remodeling process that is characterized by myocyte hypertrophy, myocyte death and fibrosis, resulting in impaired cardiac function and heart failure. Cardiac remodeling is associated with derepression of genes that contribute to disease progression. This review focuses on evidence linking members of the Ca2+/calmodulin-dependent protein kinase (CaMK) superfamily, specifically CaMKII, protein kinase D (PKD) and microtubule associated kinase (MARK), to stress-induced derepression of pathological cardiac gene expression through their effects on class Ha histone deacetylases (HDACs). (c) 2006 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.

引用

页码：667 / 677

页数：11

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