Tutorial 凝血机制--血小板的补丁之路-- VWF因子（启动凝血，血小板导航）_哔哩哔哩_bilibili
Platelet navigation factor, the largest coagulation factor, with a half-life of 10-24h
After vascular injury, components that were originally not exposed—vWF and collagen fibers—are revealed.
vWF mediates the adhesion of platelets to the injured sites on the vascular endothelium, then initiates fibrin network formation.
Source
80-85% from endothelial cells
15-20% produced by megakaryocytes, stored in platelets and released upon platelet activation
Structure
Composed of many monomers connected together, different monomers have different structures and functions (such as binding coagulation factors and protecting coagulation factors)
They often assemble into 20-200 dimers to form long chains, which twist together (similar to a ball of yarn). Many binding sites are present on these chains. Under normal blood flow conditions, these chains are usually coiled with binding sites hidden inside and do not promote coagulation. When blood flow creates vortices, the chains are unraveled, exposing the binding sites which can bind many substances and promote coagulation.
ADAMTS13 can cleave vWF to control its length. If ADAMTS13 is abnormal and cannot cleave, thrombosis is prone to occur ([[Thrombotic Thrombocytopenic Purpura|TTP]]), often occurring in the brain and kidneys—areas with high blood flow volume, high blood flow velocity, and great shear force, making vWF more likely to unfold. Lack of ADAMTS13 in these conditions makes thrombosis more likely.