Colman R W, Schmaier A H
Crit Rev Oncol Hematol. 1986;5(1):57-85. doi: 10.1016/s1040-8428(86)80053-1.
This review is intended to be a critical state-of-the-art overview of the activation and inhibition of the proteins (factor XII, prekallikrein, high molecular weight kininogen, and factor XI) of the contact phase of coagulation. Specifically, this review will reconsider the concept of the reciprocal activation of the proteases of the contact phase of coagulation, factor XII, and prekallikrein, in light of much recent evidence indicating that factor XII, itself, autoactivates when associated with negatively charged surfaces. In addition, the mechanisms for amplification of activation of the proteins of the contact phase of coagulation will be discussed from the pivotal role of high molecular weight kininogen, or one of its altered forms, serving as a cofactor to order the activation of the zymogens it is associated with. The role and relative importance of each of the naturally occurring plasma protease inhibitors (C1-inhibitor, alpha-2-macroglobulin, alpha-1-antitrypsin, antithrombin III, and alpha-1-antiplasmin) will be assessed as they relate to the dampening of contact phase activation. Finally, the contact phase of coagulation activation will be discussed not only as a plasma proteolytic mechanism, but also as it interacts with platelets.
本综述旨在对凝血接触相蛋白（因子 XII、前激肽释放酶、高分子量激肽原和因子 XI）的激活和抑制进行批判性的最新概述。具体而言，鉴于最近大量证据表明因子 XII 本身在与带负电荷表面结合时会自动激活，本综述将重新审视凝血接触相蛋白酶（因子 XII 和前激肽释放酶）相互激活的概念。此外，将从高分子量激肽原或其一种变体形式作为辅因子来有序激活与其相关的酶原的关键作用，讨论凝血接触相蛋白激活的放大机制。将评估每种天然存在的血浆蛋白酶抑制剂（C1 抑制剂、α-2-巨球蛋白、α-1-抗胰蛋白酶、抗凝血酶 III 和 α-1-抗纤溶酶）与抑制接触相激活相关的作用和相对重要性。最后，不仅将凝血接触相激活作为一种血浆蛋白水解机制进行讨论，还将探讨其与血小板的相互作用。
