Circulation Research. 2004;94:1168-1178
doi: 10.1161/01.RES.0000127122.22685.0A
doi: 10.1161/01.RES.0000127122.22685.0A
© 2004 American Heart Association, Inc.
Reviews |
Peroxisome Proliferator-Activated Receptors and Atherogenesis
Regulators of Gene Expression in Vascular Cells
From the Department of Internal Medicine II–Cardiology (N.M.), University of Ulm, Germany, and UR545 INSERM (H.D., J.-C.F., B.S.), Départment d’Athérosclérose, Institut Pasteur de Lille, Université de Lille, France.
Correspondence to Nikolaus Marx, MD, Department of Internal Medicine II–Cardiology, University of Ulm, Robert-Koch-Str. 8, D-89081 Ulm, Germany. E-mail nikolaus.marx{at}medizin.uni-ulm.de
This Review is part of a thematic series on Nuclear Receptor Signaling, which includes the following articles:
Peroxisome Proliferator-Activated Receptors and Atherogenesis: Regulators of Gene Expression in Vascular Cells
Nuclear Receptor Signaling in the Control of Cholesterol Homeostasis
Nuclear Receptor Signaling and Cardiac Energetics
Daniel Kelly Guest Editor
A large body of data gathered over the past couple of years has identified the peroxisome proliferator-activated receptors (PPAR) 
, 
, and ß/
as transcription factors exerting modulatory actions in vascular cells. PPARs, which belong to the nuclear receptor family of ligand-activated transcription factors, were originally described as gene regulators of various metabolic pathways. Although the PPAR, , and ß/ subtypes are 
60% to 80% homologous in their ligand- and DNA-binding domains, significant differences in ligand and target gene specificities are observed. PPAR is activated by polyunsaturated fatty acids and oxidized derivatives and by lipid-modifying drugs of the fibrate family, including fenofibrate or gemfibrozil. PPAR controls expression of genes implicated in lipid metabolism. PPAR, in contrast, is a key regulator of glucose homeostasis and adipogenesis. Ligands of PPAR include naturally occurring FA derivatives, such as hydroxyoctadecadienoic acids (HODEs), prostaglandin derivatives such as 15-deoxy
12,14-prostaglandin J2, and glitazones, insulin-sensitizing drugs presently used to treat patients with type 2 diabetes. Ligands for PPARß/ are polyunsaturated fatty acids, prostaglandins, and synthetic compounds, some of which are presently in clinical development. PPARß/ stimulates fatty acid oxidation predominantly acting in muscle. All PPARs are expressed in vascular cells, where they exhibit antiinflammatory and antiatherogenic properties. In addition, studies in various animal models as well as clinical data suggest that PPAR and PPAR activators can modulate atherogenesis in vivo. At present, no data are available relating to possible effects of PPARß/ agonists on atherogenesis. Given the widespread use of PPAR and PPAR agonists in patients at high risk for cardiovascular disease, the understanding of their function in the vasculature is not only of basic interest but also has important clinical implications. This review will focus on the role of PPARs in the vasculature and summarize the present understanding of their effects on atherogenesis and its cardiovascular complications.
Key Words: peroxisome proliferator-activated receptors • vascular cells • arteriosclerosis • diabetes • lipid metabolism
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