Remodeling the blood coagulation cascade
Remodeling the blood coagulation cascade
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DOI：
10.1023/b:thro.0000014588.95061.28
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发表时间：
2003-08-01
影响因子：
4
通讯作者：
Hoffman, M
中科院分区：
文献类型：
--
作者：
Hoffman, M
凝血级联的概念描述了凝血因子的生化相互作用，但作为体内止血过程的模型存在缺陷。例如，该模型不能解释为什么血友病患者在具有完整的VIIa因子/组织因子（“外在”）途径时出血。止血需要在血管损伤部位形成不可渗透的血小板和纤维蛋白塞，但它也需要在这一过程中激活的强效促凝物质保持在损伤部位的局限性。这种对凝血的控制是通过将促凝反应定位于特定细胞表面的事件来实现的，以防止凝血在整个血管系统中扩散。考虑到细胞的关键作用，我们可以构建一个凝血模型，更好地解释体内出血和血栓形成。这种基于细胞的模型表明，“内在”和“外在”通路实际上不是冗余的系统，而是在不同的细胞表面并行运行。
The concept of a coagulation cascade describes the biochemical interactions of the coagulation factors, but has flaws as a model of the hemostatic process in vivo. For example, the model cannot explain why hemophiliacs bleed when they have an intact factor VIIa/tissue factor ("extrinsic") pathway. Hemostasis requires the formation of an impermeable platelet and fibrin plug at the site of vessel injury, but it also requires that the powerful procoagulant substances activated in this process remain localized to the site of injury. This control of blood coagulation is accomplished by localizing the procoagulant reactions to events on specific cell surfaces to keep coagulation from spreading throughout the vascular system. A consideration of the critical role of cells allows us to construct a model of coagulation that better explains bleeding and thrombosis in vivo. This cell-based model suggests that the "intrinsic" and "extrinsic" pathways are in fact not redundant systems, but operate in parallel on different cell surfaces.