Fibrinogen and red blood cells in venous thrombosis.
Fibrinogen and red blood cells in venous thrombosis.
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DOI：
10.1016/j.thromres.2014.03.017
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发表时间：
2014-05
影响因子：
7.5
通讯作者：
Wolberg AS
中科院分区：
文献类型：
--
作者：
Aleman MM;Walton BL;Byrnes JR;Wolberg AS
深静脉血栓形成和肺栓塞，统称为静脉血栓栓塞（VTE），每年影响超过100万美国人。静脉血栓栓塞是由炎症和血瘀引起的，导致形成富含纤维蛋白和红细胞的血栓。然而，关于调节纤维蛋白和红细胞进入静脉血栓的机制，以及这些成分如何调节血栓的大小或溶解，我们知之甚少。在静脉血栓栓塞患者的血浆中观察到循环纤维蛋白原升高（高纤维蛋白原血症）和纤维蛋白（原）结构和功能异常，包括纤维蛋白网络密度增加和纤维蛋白溶解抵抗。红细胞数量和/或功能异常也与静脉血栓栓塞风险有关。红细胞对静脉血栓栓塞的贡献被认为源于它们对血液粘度和血小板向血管壁边缘的影响。最近的研究表明，红细胞也表达磷脂酰丝氨酸，支持凝血酶的产生，并减少纤维蛋白溶解。红细胞与纤维蛋白（原）和细胞（包括血小板和内皮细胞）的相互作用也可能促进血栓的形成。纤维蛋白（原）和红细胞在静脉血栓栓塞的病理生理中的作用有待进一步研究。
Deep vein thrombosis and pulmonary embolism, collectively termed venous thromboembolism (VTE), affect over 1 million Americans each year. VTE is triggered by inflammation and blood stasis leading to the formation of thrombi rich in fibrin and red blood cells (RBCs). However, little is known about mechanisms regulating fibrin and RBC incorporation into venous thrombi, or how these components mediate thrombus size or resolution. Both elevated circulating fibrinogen (hyperfibrinogenemia) and abnormal fibrin(ogen) structure and function, including increased fibrin network density and resistance to fibrinolysis, have been observed in plasmas from patients with VTE. Abnormalities in RBC number and/or function have also been associated with VTE risk. RBC contributions to VTE are thought to stem from their effects on blood viscosity and margination of platelets to the vessel wall. More recent studies suggest RBCs also express phosphatidylserine, support thrombin generation, and decrease fibrinolysis. RBC interactions with fibrin(ogen) and cells, including platelets and endothelial cells, may also promote thrombus formation. The contributions of fibrin(ogen) and RBCs to the pathophysiology of VTE warrants further investigation.
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