血管性血友病因子
ADAMTS13号
止血
血管性血友病
血栓形成
医学
血栓性血小板减少性紫癜
血小板
出血时间
内科学
免疫学
心脏病学
血小板聚集
作者
Timothy C. Nichols,Dwight A. Bellinger,Elizabeth P. Merricks,Robin A. Raymer,Mark T. Kloos,Natalie DeFriess,Margaret V. Ragni,Thomas R. Griggs
出处
期刊:Thrombosis
[Hindawi Publishing Corporation]
日期:2010-02-07
卷期号:2010: 1-11
被引量:29
摘要
Use of animal models of inherited and induced von Willebrand factor (VWF) deficiency continues to advance the knowledge of VWF-related diseases: von Willebrand disease (VWD), thrombotic thrombocytopenic purpura (TTP), and coronary artery thrombosis. First, in humans, pigs, and dogs, VWF is essential for normal hemostasis; without VWF bleeding events are severe and can be fatal. Second, the ADAMTS13 cleavage site is preserved in all three species suggesting all use this mechanism for normal VWF multimer processing and that all are susceptible to TTP when ADAMTS13 function is reduced. Third, while the role of VWF in atherogenesis is debated, arterial thrombosis complicating atherosclerosis appears to be VWF-dependent. The differences in the VWF gene and protein between humans, pigs, and dogs are relatively few but important to consider in the design of VWF-focused experiments. These homologies and differences are reviewed in detail and their implications for research projects are discussed. The current status of porcine and canine VWD are also reviewed as well as their potential role in future studies of VWF-related disorders of hemostasis and thrombosis.
科研通智能强力驱动
Strongly Powered by AbleSci AI