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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:血肿和炎症中作用的证据

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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)和等离子体凝固因子VII(FVII)之间的相互作用引发了导致凝血酶产生的凝血网络和纤维蛋白凝块的形成。凝血酶还通过其激活细胞蛋白酶活化受体(PARS),其激活炎性途径的组分。 TF由心肌细胞和来自小鼠转基因的证据表达的人类TF迷你基因的证据表达了非常低的人TF,表明TF-FVII相互作用对于心脏内的血肿至关重要。 TF和FVII之间的病理接触可能在缺血再灌注(I-R)损伤期间,这可能导致凝血和凝血酶产生的激活。来自动物模型的证据现在表明凝血酶是I-R损伤中炎症的重要介质。因此,凝血途径代表了用于防止I-R损伤的新型治疗靶标。

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