Tissue factor, blood coagulation, and beyond: an overview.
Tissue factor, blood coagulation, and beyond: an overview.
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DOI：
10.4061/2011/367284
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发表时间：
2011
影响因子：
2
通讯作者：
Chu AJ
中科院分区：
文献类型：
--
作者：
Chu AJ
新的证据表明组织因子 (TF) 具有广泛的生物学功能。 TF 在启动外源性血液凝固中的经典作用及其与心血管风险密切相关的直接血栓形成作用早已确定。在许多临床情况下经常观察到的 TF 过度表达/高凝状态无疑扩大了其在促炎症、糖尿病、肥胖、心血管疾病、血管生成、肿瘤转移、伤口修复、胚胎发育、细胞粘附/迁移、先天免疫、感染、妊娠丢失等中的作用。本文广泛涵盖了开创性的观察结果，以讨论 TF 与多种疾病发展或表现相关的致病作用。从生化角度来看，细胞外 TF 信号通过蛋白酶激活受体 (PAR) 介导，引发细胞激活和炎症反应。 TF 的多种生物学作用与凝血依赖性或非凝血介导的作用相关。显然，TF 高凝状态以“自分泌”或“旁分泌”的方式为凝血-炎症-血栓形成回路提供能量，从而引发广泛的病理生理学。因此，TF 抑制、抗凝、PAR 阻断或一般抗炎为缓解不同的病理状况提供了一系列治疗益处。
Emerging evidence shows a broad spectrum of biological functions of tissue factor (TF). TF classical role in initiating the extrinsic blood coagulation and its direct thrombotic action in close relation to cardiovascular risks have long been established. TF overexpression/hypercoagulability often observed in many clinical conditions certainly expands its role in proinflammation, diabetes, obesity, cardiovascular diseases, angiogenesis, tumor metastasis, wound repairs, embryonic development, cell adhesion/migration, innate immunity, infection, pregnancy loss, and many others. This paper broadly covers seminal observations to discuss TF pathogenic roles in relation to diverse disease development or manifestation. Biochemically, extracellular TF signaling interfaced through protease-activated receptors (PARs) elicits cellular activation and inflammatory responses. TF diverse biological roles are associated with either coagulation-dependent or noncoagulation-mediated actions. Apparently, TF hypercoagulability refuels a coagulation-inflammation-thrombosis circuit in “autocrine” or “paracrine” fashions, which triggers a wide spectrum of pathophysiology. Accordingly, TF suppression, anticoagulation, PAR blockade, or general anti-inflammation offers an array of therapeutical benefits for easing diverse pathological conditions.