Wohner N
Department of Medical Biochemistry, Semmelweis University, Budapest, Hungary 1088, Puskin u. 9, Hungary.
Cardiovasc Hematol Agents Med Chem. 2008 Jul;6(3):224-8. doi: 10.2174/187152508784871972.
Although fibrin forms the core matrix of thrombi, their structure depends also on the cellular elements embedded in its meshwork. Platelets are essential in the initial stages of thrombus formation, because they adhere and aggregate at sites of blood vessel wall injury and then serve as a surface for coagulation reactions, the overall rate of which determines the final structure of fibrin. In addition, platelets affect fibrinolysis through their proteins and phospholipids, which modulate plasmin activity. Leukocytes form mixed aggregates with platelets and thus influence the structure of thrombi. After activation they secrete different proteases (elastase, cathepsin G, matrix metalloproteinases) that enhance the von Willebrand factor-dependent platelet adhesion. Leukocyte-derived enzymes, first of all elastase, effect fibrinolysis by direct digestion of fibrin or indirectly modulate it by partial degradation of zymogens and inhibitors of coagulation and fibrinolytic proteases.
尽管纤维蛋白构成血栓的核心基质，但其结构也取决于嵌入其网络中的细胞成分。血小板在血栓形成的初始阶段至关重要，因为它们在血管壁损伤部位黏附并聚集，然后作为凝血反应的表面，凝血反应的总体速率决定了纤维蛋白的最终结构。此外，血小板通过其蛋白质和磷脂影响纤维蛋白溶解，这些蛋白质和磷脂调节纤溶酶活性。白细胞与血小板形成混合聚集体，从而影响血栓的结构。激活后，它们分泌不同的蛋白酶（弹性蛋白酶、组织蛋白酶G、基质金属蛋白酶），增强血管性血友病因子依赖性血小板黏附。白细胞衍生的酶，首先是弹性蛋白酶，通过直接消化纤维蛋白影响纤维蛋白溶解，或通过部分降解凝血酶原以及凝血和纤维蛋白溶解蛋白酶的抑制剂间接调节纤维蛋白溶解。
