Wu Kenneth K, Matijevic-Aleksic Nena
Biology Division of Hematology and Vascular Research Center, University of Texas Health Science Center, Houston, TX 77030, USA.
Crit Rev Clin Lab Sci. 2005;42(3):249-77. doi: 10.1080/10408360590951171.
There have been major advances in our understanding of thrombosis and antithrombotic drugs. This review focuses on the molecular aspects of thrombus formation and antithrombotic therapy. Molecules involved in arterial thrombosis are derived from inflammatory cells in the atherosclerotic plaque and blood platelets. These molecules work in concert to promote plaque instability and thrombogenicity. Thrombus formation on the ruptured plaque is mediated by platelet and coagulation activation. By contrast, molecules involved in venous thrombosis are derived from the activated coagulation cascade. Platelets appear to play a secondary role. The antithrombotic drugs are classified according to their targeted constituents: antiplatelet agents and anticoagulants; the latter are further divided into non-specific anticoagulants, such as vitamin K antagonists and heparin, and direct thrombin inhibitors, including hirudin and argatroban. Currently available antiplatelet agents target glycoprotein IIbIIIa (abciximab, tirofiban, eptifibatide), cyclooxygenase-1 (aspirin) or adenosine diphosphate receptor, P2Y12 (clopidogrel).
我们对血栓形成和抗血栓药物的理解取得了重大进展。本综述聚焦于血栓形成和抗血栓治疗的分子层面。参与动脉血栓形成的分子源自动脉粥样硬化斑块中的炎症细胞和血小板。这些分子协同作用，促进斑块不稳定和血栓形成倾向。破裂斑块上的血栓形成由血小板和凝血激活介导。相比之下，参与静脉血栓形成的分子源自激活的凝血级联反应。血小板似乎起次要作用。抗血栓药物根据其靶向成分分类：抗血小板药物和抗凝剂；后者进一步分为非特异性抗凝剂，如维生素K拮抗剂和肝素，以及直接凝血酶抑制剂，包括水蛭素和阿加曲班。目前可用的抗血小板药物靶向糖蛋白IIbIIIa（阿昔单抗、替罗非班、依替巴肽）、环氧合酶-1（阿司匹林）或二磷酸腺苷受体P2Y12（氯吡格雷）。
