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Cardiovascular Research 2005 66(3):423-426; doi:10.1016/j.cardiores.2005.03.023
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Copyright © 2005, European Society of Cardiology

Fatty acid oxidation inhibition with PPAR{alpha} activation (FOXIB/PPAR{alpha}) for normalizing gene expression in heart failure?

Heinz Rupp*, Thomas P. Rupp and Bernhard Maisch

Molecular Cardiology Laboratory, Department of Internal Medicine and Cardiology, Philipps University of Marburg, Marburg, Germany

* Corresponding author. Molecular Cardiology Laboratory, Department of Internal Medicine and Cardiology, Karl-von-Frisch-Strasse 1, 35033 Marburg, Germany. Tel.: +49 6421 286 5032; fax: +49 6421 286 8964. Email address: Rupp@staff.uni-marburg.de

Received 23 March 2005; accepted 31 March 2005

The first 150 words of the full text of this article appear below.

See also article by Lionetti et al. [7] (pages 454–461) in this issue.


   1. Gene expression of overloaded cardiomyocytes
 
In the majority of patients with heart failure, the left ventricle is overloaded and cardiac hypertrophy occurs, which is associated with a dysregulated gene expression. A hallmark of hypertrophied animal hearts is the fetal phenotype, which has been characterized on the basis of a reduced or inadequate expression of {alpha}-myosin heavy chain ({alpha}-MHC) and the Ca2+ pump (SERCA2) of the sarcoplasmic reticulum (SR) that appears to be a marker of a great number of dysregulated genes [1] also involving Na+–Ca2+ exchange [2]. During progression of heart failure involving neuroendocrine activation, reprogramming of an even larger group of genes ensues. Microarray data has revealed at least 251 genes that are up- or downregulated upon heart failure [3]. The finding that many of the differentially expressed genes code for enzymes involved in energy metabolism might . . . [Full Text of this Article]


   2. Oxfenicine treatment in a dog model of ischemic heart failure
 

   3. Etomoxir counteracts a dysregulated gene expression of overloaded cardiomyocytes
 

   4. CPT I inhibition in patients with heart failure
 

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