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Comparative and Functional Genomics
Volume 5, Issue 6-7, Pages 459-470
Research article

Identification of a Core Set of Genes That Signifies Pathways Underlying Cardiac Hypertrophy

1CHARC (Copenhagen Heart Arrhythmia Research Center), Department of Medicine B, H: S Rigshospitalet, University of Copenhagen Medical School, 20 Juliane Mariesvej, Copenhagen, DK 2100, Denmark
2Molecular Diagnostic Laboratory, Department of Clinical Biochemistry, Aarhus University Hospital, Denmark
3Center for Biological Sequence Analysis, Technical University of Denmark, Lyngby, Kgs 2800, Denmark
4Department of Pharmacology, Copenhagen University, Copenhagen 2100, Denmark

Received 6 February 2004; Revised 30 August 2004; Accepted 21 September 2004

Copyright © 2004 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Although the molecular signals underlying cardiac hypertrophy have been the subject of intense investigation, the extent of common and distinct gene regulation between different forms of cardiac hypertrophy remains unclear. We hypothesized that a general and comparative analysis of hypertrophic gene expression, using microarray technology in multiple models of cardiac hypertrophy, including aortic banding, myocardial infarction, an arteriovenous shunt and pharmacologically induced hypertrophy, would uncover networks of conserved hypertrophy-specific genes and identify novel genes involved in hypertrophic signalling. From gene expression analyses (8740 probe sets, n = 46) of rat ventricular RNA, we identified a core set of 139 genes with consistent differential expression in all hypertrophy models as compared to their controls, including 78 genes not previously associated with hypertrophy and 61 genes whose altered expression had previously been reported. We identified a single common gene program underlying hypertrophic remodelling, regardless of how the hypertrophy was induced. These genes constitute the molecular basis for the existence of one main form of cardiac hypertrophy and may be useful for prediction of a common therapeutic approach. Supplementary material for this article can be found at: