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Cardiovascular Research 2007 73(4):667-677; doi:10.1016/j.cardiores.2006.11.036
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Copyright © 2007, European Society of Cardiology

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

Timothy A. McKinsey*

Myogen, Inc./Gilead Colorado, Inc., 7575 West 103rd Ave., Westminster, Colorado 80021, USA

* Tel.: +1 303 533 1736; fax: +1 303 410 6669. Email address: timothy.mckinsey{at}gilead.com

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 IIa histone deacetylases (HDACs).

KEYWORDS Transcription; Signaling; CaM kinase; Histone deacetylase; Chromatin

Time for primary review 27 days


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