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Inhibiting the intrinsic pathway of coagulation with a FXII-targeting RNA Aptamer

机译:靶向FXII的RNA适体抑制凝血的内在途径

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摘要

BackgroundExposure of the plasma protein factor XII to an anionic surface generates activated factor XII that not only triggers the intrinsic pathway of blood coagulation through the activatio of factor XI, but also mediates various vascular responses through activation of the plasma contact system. While deficiencies of factor XII are not associated with excessive bleeding, thrombosis models in factor deficient animals have suggested that this protein contributes to stable thrombus formation. Therefore, factor XII has emerged as an attractive therapeutic target to treat or prevent pathological thrombosis formation without increasing the risk for hemorrhage.
机译:背景血浆蛋白因子XII暴露于阴离子表面会产生激活的因子XII,该因子不仅通过因子XI的激活触发凝血的内在途径,而且通过激活血浆接触系统介导各种血管反应。虽然因子XII的缺乏与出血过多无关,但因子缺乏动物的血栓形成模型表明该蛋白有助于稳定的血栓形成。因此,因子XII已成为治疗或预防病理性血栓形成而不增加出血风险的有吸引力的治疗靶标。

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