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Blood, 1 November 2008, Vol. 112, No. 9, pp. 3555-3562. Prepublished online as a Blood First Edition Paper on August 1, 2008; DOI 10.1182/blood-2008-04-144758. This Article Full Text (PDF) All Versions of this Article: blood-2008-04-144758v1 112/9/3555    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Stoll, G. Articles by Nieswandt, B. Search for Related Content PubMed PubMed Citation Articles by Stoll, G. Articles by Nieswandt, B. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted April 24, 2008 Accepted July 23, 2008 Molecular mechanisms of thrombus formation in ischemic stroke: novel insights and targets for treatment Guido Stoll, Christoph Kleinschnitz, and Bernhard Nieswandt* Department of Neurology, University of Wurzburg, Wurzburg, Germany Vascular Biology, University of Wurzburg, Wurzburg, Germany * Corresponding author; email: bernhard.nieswandt{at}virchow.uni-wuerzburg.de. In ischemic stroke treatment options are limited. Therapeutic thrombolysis is restricted to the first few hours after stroke, and the utility of current platelet aggregation inhibitors including GPIIb/IIIa receptor antagonists, and anticoagulants is counterbalanced by the risk of intracerebral bleeding complications. Numerous attempts to establish neuroprotection in ischemic stroke have been unfruitful. Thus, there is strong demand for novel treatment strategies. Major advances have been made in understanding the molecular functions of platelet receptors such as glycoprotein (GP)Ib and GPVI and their downstream signaling pathways which allows interference with their function. Inhibition of these receptors in the mouse stroke model of transient middle cerebral artery occlusion prevented infarctions in vivo without increasing the risk of intracerebral bleeding. Similarly, it is now clear that the intrinsic coagulation factors (F)XII and FXI play a functional role in thrombus formation and stabilization during stroke: their deficiency or blockade protects from cerebral ischemia without overtly affecting hemostasis. Based on the accumulating evidence that thrombus formation and hemostasis are not inevitably linked, new concepts for prevention and treatment of ischemic stroke may eventually emerge without the hazard of severe bleeding complications. This review discusses recent advances related to antithrombotic strategies in experimental stroke research. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. Kleinschnitz, S. F. De Meyer, T. Schwarz, M. Austinat, K. Vanhoorelbeke, B. Nieswandt, H. Deckmyn, and G. Stoll Deficiency of von Willebrand factor protects mice from ischemic stroke Blood, April 9, 2009; 113(15): 3600 - 3603. [Abstract] [Full Text] [PDF]

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