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(Circulation Research. 2002;91:373.)
© 2002 American Heart Association, Inc.

Editorials

PPAR and Vascular Inflammation

Adding Another Piece to the Puzzle

Nikolaus Marx

From the Department of Internal Medicine II, Cardiology, University of Ulm, Germany.

Correspondence to Nikolaus Marx, MD, Dept of Internal Medicine II, Cardiology, University of Ulm, Robert-Koch-Str. 8, D-89081 Ulm, Germany. E-mail nikolaus.marx@medizin.uni-ulm.de

Key Words: arteriosclerosis • peroxisome proliferator-activated receptor • CCAAT/enhancer-binding protein • inflammation • vascular smooth muscle cells

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Work in basic science and clinical research over the last decades has led to our present understanding of arteriosclerosis as an inflammatory disease in the vessel wall. As such, lesion development is characterized by the presence of inflammatory cells like monocytes and T cells, the release of proinflammatory cytokines like interleukin (IL)-6 and tumor necrosis factor (TNF), as well as by the activation of vascular smooth muscle cells (VSMCs).¹ This inflammatory environment can ultimately result in unstable, vulnerable lesions, which are prone to rupture, thus potentially causing acute coronary syndromes.² Given the present view of atherogenesis, research in vascular biology has focussed on strategies to modulate this inflammatory process in the vessel wall. Among those approaches, activators of the ligand-activated nuclear transcription factor peroxisome proliferator-activated receptor (PPAR) have emerged as a promising tool to influence inflammation in the vasculature. Originally identified as master regulators in adipogenesis and glucose homeostasis (reviewed in Auwerx³), work from the last couple of years has shown that PPAR is expressed in vascular cells in vivo and in vitro, and that activators of PPAR may exhibit antiinflammatory properties in these cells. In monocytes/macrophages, PPAR activators inhibit the release of proinflammatory cytokines and matrix-degrading enzymes; in endothelial cells, they modulate the expression of chemokines and endothelin; and in T cells, PPAR ligands have been shown to reduce the secretion of IFN-. Moreover, in VSMCs, PPAR inhibits migration and proliferation and decreases the release of matrix metalloproteinases. In vivo experiments in mouse models of arteriosclerosis . . . [Full Text of this Article]

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