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STATE-OF-THE-ART PAPER

Peroxisome Proliferator-Activated Receptors at the Crossroads of Obesity, Diabetes, and Cardiovascular Disease

Andries J. Gilde, PhD^_*,, Jean-Charles Fruchart, PhD^_*,, and Bart Staels, PhD^_*,,,_*

^_* INSERM U545, Institut Pasteur de Lille, France
Department of Atherosclerosis, Institut Pasteur de Lille, France
University of Lille 2, Lille, France.

Manuscript received November 29, 2005; revised manuscript received April 11, 2006, accepted April 18, 2006.

^_* Reprint requests and correspondence: Dr. Bart Staels, U545 INSERM, Institut Pasteur de Lille, 1 Rue du Professor Calmette B.P. 245, Lille, F-59019 France. (Email: Bart.Staels{at}pasteur-lille.fr).

Since their discovery in the early 1990s, the members of the peroxisome proliferator-activated receptor (PPAR) subfamily of nuclear receptors have been recognized as therapeutic targets against dyslipidemia and diabetes. Recent studies also identified anti-inflammatory actions of PPARs in cells constituting the atherosclerotic lesion. Delineation of this activity extended the therapeutic potential of PPAR activators beyond their original design as metabolic controllers. The PPAR family consists of 3 PPAR isoforms: , ß/, and , which exert different and sometimes overlapping effects on whole-body physiology in particular on lipid and glucose metabolism. This review summarizes the current knowledge on the role of PPARs in cardiovascular disease, the metabolic syndrome, atherosclerosis, and cardiac function.

Abbreviations and Acronyms   CVD = cardiovascular disease   HDL = high-density lipoprotein   IL = interleukin   LDL = low-density lipoprotein   PPAR = peroxisome proliferator-activated receptors   SPPARM = selective peroxisome proliferator-activated receptors modulator   TZD = thiazolidinedione

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