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Cardiovascular Research 2005 65(4):770-771; doi:10.1016/j.cardiores.2005.01.009
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Copyright © 2005, European Society of Cardiology

Peroxisome proliferator-activated receptor β/{delta}: a new antihypertrophic drug target?

Natalia N. Petrashevskaya* and Arnold Schwarz

Institute of Molecular Pharmacology and Biophysics, Department of Surgery, University of Cincinnati College of Medicine, G936 Cardiovascular Research Center, 231 Albert Sabin Way, Cincinnati, OH 45267-0529, United States

* Corresponding author. Tel.: +1 513 558 2374; fax: +1 513 558 1778. Email address: petrasnn@email.uc.edu

Received 6 January 2005; accepted 10 January 2005

The first 10% of the full text of this article appears below.

See article by Planavila et al. [6] (pages 832–841) in this issue.

In the normal adult heart, plasticity of ATP production is provided by coordinated changes in the expression of genes involved in cellular fatty acid (FA) utilization and glucose oxidation. The phenotypes of acquired forms of heart failure in human and animal models are associated with energy substrate changes accompanying a reduced mitochondrial FA oxidative capacity and a shift to glucose metabolism, resembling the fetal metabolic program [1]. High glucose conditions, initially serving as a protective response to support contractile function, stimulate the production of angiotensin II (Ang II), a . . . [Full Text of this Article]


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