[脂蛋白(a):血栓形成和血管硬化)之间的联系。

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[脂蛋白(a):血栓形成和血管硬化)之间的联系。

地中海Pregl。2007; 1 - 2月60 (1 - 2):37-41。

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17853709 (在PubMed

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文摘

简介:众所周知,大量血栓形成机制可以参与动脉粥样硬化疾病的每一个阶段。Lp (a)脂蛋白的发现及其与纤溶酶原显示另一个致病物的结构相似性动脉粥样化形成和血栓形成之间的联系。LP (A)脂蛋白的一些特征:这种脂蛋白存在于整个人口在一个广泛的血浆浓度。它有许多不同的亚型。它发生在肝脏合成,但它实际上是新陈代谢独立于其他脂蛋白。今天,Lp (a)脂蛋白被认为是一个独立的心脏和脑缺血性疾病的危险因素。纤溶机制:纤溶机制的主要作用是防止血栓Jormation在循环,去除已形成的。血纤维蛋白溶酶中起中心作用在这个过程中,由于不活跃的酶原纤溶酶原。物其基本活化剂是组织类型纤溶酶原激活物(t-PA)和尿激酶纤溶酶原激活物(u-PA)。最重要的抑制剂纤溶酶原是alpha2-antiplasmin物和纤溶酶原激活物抑制剂1和2 (PA-1和PAI-2)。 Structural similarity of Lp(a) and plasminogen The apo(a) and plasminogen genes are very closely linked on the long arm of chromosome 6. Because of that they are structuraly very similar and they have a cross immunological reactivity. Their common elements are so-called "kringle" structures. The key difference in structure of Lp(a) and plasminogen is replacement of Arg with Ser at position 560. This prevents splitting of apo(a) by plasminogen activators. LP(A) AND FIBRINOLYSIS: Lp(a) lipoprotein inhibits activation of plasminogen by streptokinase. It is also a competitive inhibitor of plasminogen for its binding to plasminogen receptors. Furthermore, it successfully achieves competitive inhibition of plasminogen for binding to tetranectin and thrombospondin. Also, Lp(a) inhibits activation of transforming growth factor alpha (TGF-alpha). It positively correlates with PAI-1 and it is assumed that it promotes release of tissue factor pathway inhibitor (17FPI) from endothelial cell surfaces. CONCLUSION: In regulation of the hemostatic system via apolipoprotein(a) antifibrinolytic effects, Lp(a) lipoprotein ojfers a molecular solution to the link between thrombogenesis and atherogenesis.

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药物靶点

药物	目标	类	生物	药理作用	行动
Tenecteplase	Tetranectin	蛋白质	人类	未知的	不可用	细节