Reviews |
From the Rudolf Virchow Center (U.J.H.S., B.N.), Deutsche Forschungsgemeinschaft Research Center for Experimental Biomedicine, University of Würzburg; Institute for Clinical Immunology and Transfusion Medicine (U.J.H.S.), Justus Liebig University, Giessen; and Institute of Clinical Biochemistry and Pathobiochemistry (B.N.), University of Würzburg, Germany.
Correspondence to Bernhard Nieswandt, PhD, Vascular Biology, Rudolf Virchow Center for Experimental Biomedicine, University of Würzburg, Versbacher Str. 9, 97078 Würzburg, Germany. E-mail bernhard.nieswandt{at}virchow.uni-wuerzburg.de
This Review is part of a thematic series on Mechanisms, Models, and In Vivo Imaging of Thrombus Formation, which includes the following articles:
Activation of Platelet Function Through G ProteinCoupled Receptors
Platelets As Immune Cells: Bridging Inflammation and Cardiovascular Disease
In Vivo Thrombus Formation in Murine Models
Clinical Aspects of Platelet Inhibitors and Thrombus Formation
Platelet Adhesion
Bernhard Nieswandt and Ulrich Walter Guest Editors
Platelets play a central role in hemostasis, but also in atherothrombosis, as they rapidly adhere to tissue and to one another as a response to any vascular injury. This process involves a large number of surface receptors, signaling pathways, and enzymatic cascades as well as their complex interplay. Although in vitro experiments proved successful in both identifying new receptors and pathways and developing potent and selective antithrombotic drugs, in vitro research cannot mimic the myriad hemodynamic and spatiotemporal cellular and molecular interactions that occur during the generation and propagation of thrombi in vivo. Animal models, and, with the availability of genetically modified mouse strains and of modern intravital imaging techniques, mouse models in particular, have opened new ways to identify both individual roles and the interplay of platelet proteins in complex in vivo settings. In vivo models revealed the important role of, eg, Gas6 or blood coagulation factor XII in thrombus formation, and results obtained in in vivo models raised the interesting possibility that (physiologic) hemostasis and (pathologic) thrombosis might represent 2 mechanistically different processes. This review summarizes in vivo findings that contributed significantly to our understanding of hemostatic and thrombotic processes and which may help to guide future research.
Key Words: thrombosis in vivo models platelets
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