Format

Send to

Choose Destination
See comment in PubMed Commons below
Thromb Res. 2014 Mar;133(3):308-14. doi: 10.1016/j.thromres.2013.11.007. Epub 2013 Nov 16.

Role of multiligand/RAGE axis in platelet activation.

Author information

  • 1Department 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.
  • 2Biomedical Research Laboratories, Medicine Faculty, Catholic University of Maule, Talca, Chile. Electronic address: arojasr@ucm.cl.
  • 3Department 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. Electronic address: ipalomo@utalca.cl.

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 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.

KEYWORDS:

AGEs; HMGB1; Platelets; RAGE; S100

PMID:
24296115
DOI:
10.1016/j.thromres.2013.11.007
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center