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Tissue Factor in the Myocardium: Evidence of Roles in Haemostasis and Inflammation

机译:心肌中的组织因子:止血和炎症作用的证据。

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摘要

The interaction between cell-surface tissue factor (TF) and the plasma coagulation factor VII (FVII) initiates the coagulation network that leads to the generation of thrombin and the formation of a fibrin clot. Thrombin also activates cellular protease activated receptors (PARs) through which it activates components of the inflammatory pathway. TF is expressed constitutively by cardiomyocytes and evidence from mice transgenic for a human TF mini-gene that express very low levels of human TF suggests that the TF-FVII interaction is critical for haemostasis within the heart. Pathological contact between TF and FVII may occur in the heart during ischaemia-reperfusion (I-R) injury and this may lead to activation of coagulation and thrombin generation. Evidence from animal models now suggests that thrombin is an important mediator of inflammation in I-R injury. The coagulation pathway therefore represents a novel therapeutic target for intervention in the prevention of I-R injury.
机译:细胞表面组织因子(TF)和血浆凝血因子VII(FVII)之间的相互作用启动了凝血网络,导致凝血酶的产生和血纤蛋白凝块的形成。凝血酶还激活细胞蛋白酶激活受体(PAR),通过它激活炎症途径的成分。 TF由心肌细胞组成型表达,转基因小鼠的人类TF小基因表达的证据表明,其表达的人TF水平非常低,这表明TF-FVII相互作用对于心脏内的止血至关重要。缺血和再灌注(I-R)损伤期间,心脏中可能发生TF和FVII之间的病理接触,这可能导致凝血激活和凝血酶生成。现在来自动物模型的证据表明,凝血酶是I-R损伤中炎症的重要介质。因此,凝血途径代表了用于预防I-R损伤的新型治疗靶标。

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