Tissue Factor, Thrombosis, and Chronic Kidney Disease.

Tissue Factor, Thrombosis, and Chronic Kidney Disease.
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DOI:
10.3390/biomedicines10112737
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发表时间:
2022-10-28
期刊:
影响因子:
4.7
通讯作者:
--
中科院分区:
工程技术3区
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凝血异常在慢性肾脏病(CKD)中很常见。组织因子(TF,即因子III)是外源性凝血系统的主要调节因子,可激活下游凝血蛋白酶,如因子Xa和凝血酶,并促进纤维蛋白的形成。TF和凝血蛋白酶还能激活蛋白酶激活受体(PARs),并与多种器官损伤有关。近期研究揭示了在CKD特定条件下血栓形成倾向增加的机制。硫酸吲哚酚和犬尿氨酸等尿毒症毒素在CKD中蓄积,可激活TF和凝血过程;此外,TF - 凝血蛋白酶 - PAR通路会增强炎症和纤维化,从而加剧肾损伤。在此,我们回顾近期的研究,以了解TF在增加血栓风险和CKD进展中的作用。
Coagulation abnormalities are common in chronic kidney disease (CKD). Tissue factor (TF, factor III) is a master regulator of the extrinsic coagulation system, activating downstream coagulation proteases, such as factor Xa and thrombin, and promoting fibrin formation. TF and coagulation proteases also activate protease-activated receptors (PARs) and are implicated in various organ injuries. Recent studies have shown the mechanisms by which thrombotic tendency is increased under CKD-specific conditions. Uremic toxins, such as indoxyl sulfate and kynurenine, are accumulated in CKD and activate TF and coagulation; in addition, the TF–coagulation protease–PAR pathway enhances inflammation and fibrosis, thereby exacerbating renal injury. Herein, we review the recent research studies to understand the role of TF in increasing the thrombotic risk and CKD progression.
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