Immune-mediated and lipid-mediated platelet function in atherosclerosis.
OBJECTIVE
Cardiovascular disease (CVD) is the leading cause of death and morbidity worldwide. Detailed knowledge of the mechanisms of atherosclerosis, the main underlying disease of CVD, will enable improved preventive and therapeutic options, thus potentially limiting the burden of vascular disease in aging societies. A large body of evidence illustrates the contribution of platelets to processes beyond their traditionally recognized role as mediators in thrombosis and hemostasis. Recent advances in molecular biology help to understand the complexity of atherosclerosis.


RESULTS
This article outlines the role of platelets as modulators of immune responses in the context of atherosclerosis. It provides a short overview of interactions between platelets and endothelial cells or immune cells via direct cell contact or soluble factors during atherogenesis. By means of some well examined, exemplary pathways (e.g. CD40/CD40L dyad), this article will discuss recent discoveries in immune-related function of platelets. We also focus on the relationship between platelets and the lipid metabolism highlighting potential consequences to atherosclerosis and dyslipidemia.


CONCLUSIONS
A better understanding of the molecular mechanisms of platelet-related immune activity allows their utilization as powerful diagnostic tools or targets of therapeutic intervention. Those findings might help to develop new classes of drugs which may supplement or replace classical anticoagulants and help clinicians to tackle CVD more efficiently.
aInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-University Munich, Munich, Germany bDZHK (German Centre for Cardiovascular Research), Partner Site Munich Heart Alliance, Munich, Germany.
Maiwand
M
Ahmadsei
Dirk
D
Lievens
Christian
C
Weber
Philipp
P
von Hundelshausen
Norbert
N
Gerdes
D000818:Animals; D050197:Atherosclerosis / Q000188:drug therapy / Q000276:immunology* / Q000378:metabolism; D001792:Blood Platelets / Q000502:physiology*; D019013:CD40 Antigens / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism; D006801:Humans; D050356:Lipid Metabolism; D015539:Platelet Activation; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D015398:Signal Transduction
D019013:CD40 Antigens; D015815:Cell Adhesion Molecules; D010975:Platelet Aggregation Inhibitors