Back to basics: the coagulation pathway.

IF 2.3 Q2 HEMATOLOGY Blood Research Pub Date : 2024-10-28 DOI:10.1007/s44313-024-00040-8
Seonyang Park, Joo Kyung Park
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Abstract

The classic coagulation cascade model of intrinsic and extrinsic coagulation pathways, i.e. contact activation pathway and tissue factor pathway, has been widely modified. The cascade can be categorized as follows: 1) initiation by tissue factor (TF), 2) amplification by the intrinsic tenase complex, and 3) propagation on activated platelets. TF-FVIIa forms an extrinsic tenase complex and activates FX to FXa and FIX to FIXa. FXa-FVa forms a prothrombinase complex that converts prothrombin into thrombin. At this initial stage of coagulation, only small amounts of thrombin are generated owing to the low circulating levels of FVa. The generated thrombin, although in minor quantities, is sufficient to prime the subsequent coagulation reactions. Platelets and in turn FV, FVIII, and FXI are activated. Subsequently, FVIIIa binds to FIXa to form the intrinsic tenase complex, which is aided by a cofactor, FVIIIa, and activates FX at a rate 50-times higher than that of the extrinsic tenase complex, thereby amplifying thrombin generation. Thrombin cleaves fibrinogen into one fibrin monomer and two fibrinopeptides. Fibrin monomers aggregate, crosslink, and branch into an insoluble fibrin network structure. The contact activation system is initiated by FXII, which is activated upon exposure to negatively charged surfaces. Coagulation is driven by FXIIa-mediated FXI cleavage. FXIa activates FIX, which forms an intrinsic tenase complex, eventually leading to thrombin formation. The contact activation system is considered to contribute to thrombosis but is not required for hemostasis in vivo.

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返璞归真:凝血途径。
经典的凝血级联模型包括内在和外在凝血途径,即接触活化途径和组织因子途径。级联可分为以下几类:1) 由组织因子(TF)启动,2) 由内在十肽酶复合物放大,3) 在活化的血小板上传播。TF-FVIIa 形成外在十肽酶复合物,将 FX 活化为 FXa,将 FIX 活化为 FIXa。FXa-FVa 形成凝血酶原酶复合物,将凝血酶原转化为凝血酶。在凝血的这一初始阶段,由于循环中的 FVa 水平较低,只产生少量凝血酶。生成的凝血酶虽然数量很少,但足以为随后的凝血反应提供能量。血小板进而激活 FV、FVIII 和 FXI。随后,FVIIIa 与 FIXa 结合形成内在十肽酶复合物,该复合物在辅助因子 FVIIIa 的帮助下,以高于外在十肽酶复合物 50 倍的速度激活 FX,从而扩大了凝血酶的生成。凝血酶将纤维蛋白原分解成一个纤维蛋白单体和两个纤维蛋白肽。纤维蛋白单体聚集、交联并分支成不溶性纤维蛋白网络结构。接触活化系统由 FXII 启动,FXII 在接触带负电荷的表面时被激活。凝血由 FXIIa 介导的 FXI 裂解驱动。FXIa 激活 FIX,FIX 形成内在的十肽酶复合物,最终导致凝血酶的形成。接触活化系统被认为有助于血栓形成,但并非体内止血所必需。
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来源期刊
Blood Research
Blood Research HEMATOLOGY-
CiteScore
3.70
自引率
0.00%
发文量
64
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