Department of Clinical Biochemistry and Immunohematology, Faculty of Health Sciences, Interdisciplinary Excellence Research Program on Healthy Aging (PIEI-ES), Universidad de Talca, Talca, Chile; Centro de Estudios en Alimentos Procesados (CEAP), CONICYT-Regional, Gore Maule, R09I2001, Talca, Chile.
Biomedical Research Laboratories, Medicine Faculty, Catholic University of Maule, Talca, Chile.
Thromb Res. 2014 Mar;133(3):308-14. doi: 10.1016/j.thromres.2013.11.007. Epub 2013 Nov 16.
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 β, 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.
在斑块进展的情况下，与高脂血症相关的血小板过度活跃会导致血栓形成状态的发展。在这种情况下，已经证明，晚期糖基化终产物（AGEs）显著增加血小板激活和血小板表面膜上的 AGEs 受体（RAGE）表达。除了 AGEs 之外，RAGE 的其他配体（S100、HMGB1 和淀粉样β等）在血小板激活中引起了特别关注。因此，在本文中，我们通过 RAGE 非依赖性和 RAGE 依赖性途径描述了 AGEs 引起的血小板过度活跃。
