Abstract

In the context of plaque progression, platelet hyperactivity associated with hyperlipidemia contributes to the development of a pro-thrombotic state. In this context, it has been demonstrated that advanced glycation end products (AGEs) significantly increases platelet activation and receptor for AGEs (RAGE) expression at the platelet surface membrane. In addition to AGEs, other ligands (S100, HMGB1 and amyloid beta, among others) of RAGE have raised particular attention in platelet activation. Therefore, in this article we describe platelet hyperactivity by AGEs via RAGE-independent and RAGE-dependent pathways. (C) 2013 Elsevier Ltd. All rights reserved.