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Spinelli SL, O'Brien JJ, Bancos S, et al. The PPAR-Platelet Connection: Modulators of Inflammation and Potential Cardiovascular Effects. PPAR Res. 2008;2008:328172doi: 10.1155/2008/328172.
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. (2008). The PPAR-Platelet Connection: Modulators of Inflammation and Potential Cardiovascular Effects. PPAR research, 2008328172. https://doi.org/10.1155/2008/328172
Spinelli, S L, et al. "The PPAR-Platelet Connection: Modulators of Inflammation and Potential Cardiovascular Effects." PPAR research vol. 2008 (2008): 328172. doi: https://doi.org/10.1155/2008/328172
Spinelli SL, O'Brien JJ, Bancos S, Lehmann GM, Springer DL, Blumberg N, Francis CW, Taubman MB, Phipps RP. The PPAR-Platelet Connection: Modulators of Inflammation and Potential Cardiovascular Effects. PPAR Res. 2008;2008:328172. doi: 10.1155/2008/328172. PMID: 18288284; PMCID: PMC2233896.
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PPAR Res. 2008;2008:328172. doi: 10.1155/2008/328172.

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

PPAR research

S L Spinelli, J J O'Brien, S Bancos, G M Lehmann, D L Springer, N Blumberg, C W Francis, M B Taubman, R P Phipps

Affiliations

  1. Department of Pathology and Laboratory Medicine, University of Rochester Medical Center, 601 Elmwood Avenue, Box 608, Rochester,NY 14642,USA.

PMID: 18288284 PMCID: PMC2233896 DOI: 10.1155/2008/328172

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 (PPARbeta/delta and PPARgamma) 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.

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