Altmann Johanna, Sharma Smriti, Lang Irene M
a Division of Cardiology, Department of Internal Medicine II , Vienna General Hospital, Medical University of Vienna , Vienna , Austria.
Expert Rev Hematol. 2016 Jan;9(1):69-78. doi: 10.1586/17474086.2016.1112264. Epub 2015 Dec 2.
Traditionally, venous thrombosis has been seen as the consequence of a regulated cascade of proteolytic steps leading to the polymerization of fibrinogen and fibrin crosslinking that is facilitated by platelets. A new view of thrombosis is providing a more integrated concept, with components of the vascular wall contributing to the vascular remodeling of thrombosis. Angiogenesis and inflammation are two key mechanisms that safeguard venous thrombus resolution and restitution of vascular patency after thrombosis. Disturbance of these processes leads to thrombus persistence and has potentially severe consequences for affected patients. Examples for clinical conditions associated with recurrent or persisting venous thrombosis are post-thrombotic syndrome or chronic thromboembolic pulmonary hypertension. Recently, studies using animal models of venous thrombosis have contributed to a better understanding of thrombus non-resolution that will eventually lead to modification of current treatment concepts. For example, recent data suggest that innate immunity is involved in the modification of thrombosis.
传统上，静脉血栓形成被视为一系列受调控的蛋白水解步骤的结果，这些步骤导致纤维蛋白原聚合以及由血小板促进的纤维蛋白交联。一种新的血栓形成观点正在提供一个更综合的概念，其中血管壁成分参与血栓形成的血管重塑。血管生成和炎症是保障静脉血栓溶解以及血栓形成后血管通畅恢复的两个关键机制。这些过程的紊乱会导致血栓持续存在，并对受影响的患者产生潜在的严重后果。与复发性或持续性静脉血栓形成相关的临床病症包括血栓形成后综合征或慢性血栓栓塞性肺动脉高压。最近，使用静脉血栓形成动物模型的研究有助于更好地理解血栓不溶解现象，这最终将导致对当前治疗概念的修正。例如，最近的数据表明先天免疫参与了血栓形成的改变。
