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PPAR Research
Volume 2008 (2008), Article ID 328172, 16 pages
http://dx.doi.org/10.1155/2008/328172
Review Article

The PPAR-Platelet Connection: Modulators of Inflammation and Potential Cardiovascular Effects

1Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 608, Rochester, NY 14642, USA
2Department of Environmental Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
3Cell Biology and Biochemistry, K4-12, Biological Sciences Division Battelle, Pacific Northwest Division, 902 Battelle Blvd, Richland, WA 99352, USA
4M&D-Hematology/Oncology, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642, USA
5Department of Medicine, M&D-Cardiology Unit, University of Rochester Medical Center, 601 Elmwood Avenue, Box 679-ccmc, Rochester, NY 14642, USA

Received 14 August 2007; Accepted 6 November 2007

Academic Editor: Brian N. Finck

Copyright © 2008 S. L. Spinelli et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Historically, platelets were viewed as simple anucleate cells responsible for initiating thrombosis and maintaining hemostasis, but clearly they are also key mediators of inflammation and immune cell activation. An emerging body of evidence links platelet function and thrombosis to vascular inflammation. peroxisome proliferator-activated receptors (PPARs) play a major role in modulating inflammation and, interestingly, PPARs (PPAR 𝛽 / 𝛿 and PPAR 𝛾 ) were recently identified in platelets. Additionally, PPAR agonists attenuate platelet activation; an important discovery for two reasons. First, activated platelets are formidable antagonists that initiate and prolong a cascade of events that contribute to cardiovascular disease (CVD) progression. Dampening platelet release of proinflammatory mediators, including CD40 ligand (CD40L, CD154), is essential to hinder this cascade. Second, understanding the biologic importance of platelet PPARs and the mechanism(s) by which PPARs regulate platelet activation will be imperative in designing therapeutic strategies lacking the deleterious or unwanted side effects of current treatment options.