Blood: Targeting VWF prevents traumatic brain injury-induced clotting.

Traumatic brain injury-induced clotting disease (TBI-IC) can lead to life-threatening secondary intracranial bleeding.
only now know that the pathogenesis is different from that of clotting disease caused by extracranial injury and hemorrhusic shock, but the exact mechanism of occurrence is still unclear.
in the study, the researchers reported findings that validated the hypothesis that "the von Willebrand factor (VWF) released during acute TBI is inherently highly adhesionable because its plateles combined with the A1 domain have been exposed, promoting TBI-induced vascular leakage and expendable clotting."
this highly adhesion VWF can be selectively blocked by VWF A2 domain proteins to prevent TBI-ICs, improve nerve function, and minimize the risk of bleeding.
researchers confirmed that giving A2 domain proteins through intra-peritoneal injections or intravenous infusions reduced TBI-induced death by more than 50 percent and significantly improved the nerve function of C57BL/6J male mice that suffered severe lateral fluid attacks.
A2 domain protein protects endotinoblastic cells from damage induced by small bubbles outside cells, reducing TBI-induced platel platelization and microcassing, thus preventing TBI-induced high coagulation.
A2 domain protein achieves this therapeutic effect by specifically blocking the A1 domain exposed on the highly adhesive VWF released during acute TBI.
, the results show that VWF has a causal effect in the development of TBI-IC and is the therapeutic target of this life-threatening complication of TBI.
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