Thrombosis is the pathological face of the hemostatic process, and is still the major cause of death in the Western
society. Many different components have been identified that contribute to the thrombotic occlusion of the vasculature
and several therapeutic approaches have been developed to treat this severe clinical complication. In the last several years,
a number of new agents have been under (pre)clinical investigation that are targeting von Willebrand factor (VWF), a protein
that nicely exemplifies the thin line between the normal hemostatic process and an overly active system that gives rise
to thrombotic events. Indeed, several epidemiological studies have found that increased plasma levels of VWF are associated
with an increased risk for cardiovascular complications. VWF is a multimeric protein that is pertinent to the recruitment
of platelets to the growing thrombus. VWF and platelets circulate together without interacting under normal conditions,
and should combine into a thrombus selectively when necessary. This delicate process is highly regulated by various
endothelial- and plasma proteins as well as by changes in shear stress. In the present review, an update is provided
about our current knowledge on VWF as a risk factor, mediator and pharmacological target in association with thrombosis.
Keywords: Von Willebrand factor, thrombosis, risk factor, platelets, antithrombotic agents.
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