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[纤维蛋白溶解功能障碍作为血栓形成的危险因素]

[Dysfunction of fibrinolysis as a risk factor of thrombosis].

作者信息

Kołodziejczyk Joanna, Wachowicz Barbara

机构信息

Uniwersytet Lódzki, Katedra Biochemii Ogólnej.

出版信息

Pol Merkur Lekarski. 2009 Oct;27(160):341-5.

PMID:19928667
Abstract

Fibrinolytic system constitutes a part of the haemostasis responsible for the degradation of fibrin deposits. Plasminogen proenzyme, the main component of the fibrinolytic system is activated into its active enzyme form--plasmin by activators, mainly by tissue-type plasminogen activator (t-PA) and urokinase-type plasminogen activator (u-PA). t-PA is the main plasminogen activator in the intravascular fibrinolysis, whereas u-PA is rather involved in the extracellular proteolysis. Fibrinolytic activity can be regulated as well by plasminogen activation inhibition (inhibitors: PAl-1 and PAl-2) as by plasmin activity inhibition (alpha2-antiplasmin). Under physiological conditions a balance between coagulation and fibrinolysis exists, that may be altered under pathophysiological conditions. It has been reported that in the pathogenesis of many diseases, the inflammatory processes, expression of proinflammatory mediators, enhanced tissue factor level and/or impaired fibrinolysis are involved. Inflammation disturbs haemostasis and shifts the haemostatic mechanisms in favor of thrombosis. Moreover, the endothelial dysfunction may contribute to the decrease of antithrombotic properties of vessel wall endothelium. Under pathophysiological conditions where a hypofibrinolytic state occurs, impaired fibrinolysis is considered to be an additional risk factor of thrombosis.

摘要

纤维蛋白溶解系统是止血过程的一部分,负责纤维蛋白沉积物的降解。纤维蛋白溶解系统的主要成分纤溶酶原前体通过激活剂,主要是组织型纤溶酶原激活剂(t-PA)和尿激酶型纤溶酶原激活剂(u-PA),被激活为其活性酶形式——纤溶酶。t-PA是血管内纤维蛋白溶解中的主要纤溶酶原激活剂,而u-PA则更多地参与细胞外蛋白水解。纤维蛋白溶解活性既可以通过纤溶酶原激活抑制(抑制剂:PAI-1和PAI-2)来调节,也可以通过纤溶酶活性抑制(α2-抗纤溶酶)来调节。在生理条件下,凝血和纤维蛋白溶解之间存在平衡,而在病理生理条件下这种平衡可能会改变。据报道,在许多疾病的发病机制中,涉及炎症过程、促炎介质的表达、组织因子水平升高和/或纤维蛋白溶解受损。炎症会干扰止血并使止血机制向有利于血栓形成的方向转变。此外,内皮功能障碍可能导致血管壁内皮抗血栓特性降低。在发生低纤维蛋白溶解状态的病理生理条件下,纤维蛋白溶解受损被认为是血栓形成的另一个危险因素。

相似文献

1
[Dysfunction of fibrinolysis as a risk factor of thrombosis].[纤维蛋白溶解功能障碍作为血栓形成的危险因素]
Pol Merkur Lekarski. 2009 Oct;27(160):341-5.
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Pathophysiology and clinical aspects of fibrinolysis and inhibition of coagulation. Experimental and clinical studies with special reference to women on oral contraceptives and selected groups of thrombosis prone patients.纤维蛋白溶解与凝血抑制的病理生理学及临床方面。特别针对口服避孕药的女性和特定血栓易患人群的实验与临床研究。
Dan Med Bull. 1988 Feb;35(1):1-33.
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Haemostasis in oral surgery--the possible pathogenetic implications of oral fibrinolysis on bleeding. Experimental and clinical studies of the haemostatic balance in the oral cavity, with particular reference to patients with acquired and congenital defects of the coagulation system.口腔外科中的止血——口腔纤维蛋白溶解对出血可能的发病机制影响。口腔内止血平衡的实验与临床研究,尤其涉及获得性和先天性凝血系统缺陷患者。
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Molecular mechanisms of fibrinolysis and their application to fibrin-specific thrombolytic therapy.纤维蛋白溶解的分子机制及其在纤维蛋白特异性溶栓治疗中的应用。
J Cell Biochem. 1987 Feb;33(2):77-86. doi: 10.1002/jcb.240330202.
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The fibrinolytic system in neoplasia.肿瘤中的纤维蛋白溶解系统。
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Molecular basis of fibrinolysis, as relevant for thrombolytic therapy.与溶栓治疗相关的纤维蛋白溶解的分子基础。
Thromb Haemost. 1995 Jul;74(1):167-71.

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