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Coagulation Factor XII -a Key Pro-inflammatory and Pro-coagulant Protein

机译:凝血因子XII -A关键促炎和亲凝血蛋白

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Coagulation factor XII (FXII) is a multidomain serine protease that is the starter of intrinsic coagulation pathway. FXII deficiency and clinical hemostasis are not associated with bleeding, so investigators have not considered FXII important in physiology for a long time. In seeking explanation for FXII-independent physiologic hemostasis, investigators found FXII is an essential constitute of contact system that mediates procoagulation and proinflammatory via the intrinsic coagulation pathway or the Kallikrein-kinin system, respectively. Date obtained in infectious inflammation have revealed FXII mediated clotting that limited bacterial or toxin spread in early phases, and regulated fibrinolysis in later. Moreover, FXII mediated two non-infectious inflammation Hereditary angioedema (HAE) and non-specific allergy via bradykinin (BK) formation. In the coagulation, thrombosis not only is involved with coagulation, but is redefined as thrombo-inflammatory disorder. This paper reviews in detail the progresses in roles of FXII intersection between inflammation and coagulation.
机译:凝血因子XII(FXII)是一种多麦田丝氨酸蛋白酶,其是内在凝血途径的起动器。 FXII缺乏和临床止血与出血无关,因此调查人员在很长一段时间内没有考虑在生理学中重要意义。在寻求无关的生理止血的解释时,研究人员发现FXII是一种必不可少的接触系统,分别通过内在凝血途径或Kallikrein-kinin系统介导原因和促炎。在传染性炎症中获得的枣揭示了副仙介导的凝血,其中有限的细菌或毒素在早期阶段扩散,并在后面的调节纤维蛋白溶解。此外,FXII介导的两种非传染性炎症遗传性血管血液(HAE)和通过Bradykinin(BK)形成的非特异性过敏。在凝血中,血栓形成不仅涉及凝血,而且被重新定义为血栓炎症病症。本文详细介绍了FXII交点在炎症和凝血之间的作用的进展。

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