Role of von Willebrand factor (VWF), platelets, and aberrant flow in the initiation of venous thrombosis

DOI: 10.1126/sciadv.adr5250 Publication Date: 2025-02-05T18:59:36Z
ABSTRACT
Deep vein thrombosis is a major cause of morbidity and mortality worldwide. However, because the absence overt blood vessel damage, how venous actually initiated remains unclear. Using endothelialized fluidic devices, we show that aberrant flow patterns may occur in valve pockets individuals with common stasis-related risk factors can formation von Willebrand factor–platelet tangles are resistant to ADAMTS13 removal. These factor–bound platelets specifically recruit neutrophils manner dependent on platelet-activated α IIb β 3 , neutrophil SLC44A2, endothelial P-selectin. The interaction SLC44A2 activated promotes prothrombotic extracellular traps. data provide molecular cellular insights into proclivity for develop suggest an alternative strategy protect against initiation thrombosis.
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