The PPAR-Platelet Connection: Modulators of Inflammation and Potential Cardiovascular Effects. (3rd December 2007)

• Record Type: Journal Article
• Authors: Spinelli, S. L.; O'Brien, J. J.; Bancos, S.; Lehmann, G. M.; Springer, D. L.; Blumberg, N.; Francis, C. W.; Taubman, M. B.; Phipps, R. P.
• Other Names: Finck Brian N. Academic Editor.
• Is Part Of: PPAR research. Volume 2008(2008)
• Publication Date: 2007-12-03
• Subjects: Peroxisomes -- Periodicals; Peroxisomal disorders -- Periodicals; 571.65505
• DOI: 10.1155/2008/328172
• Languages: English
• ISSNs: 1687-4757

Abstract

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 (PPARβ /δ and PPARγ ) 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.