组织因子
蛋白酵素
凝结
凝血酶
肾脏疾病
纤维蛋白
医学
凝血活酶
肾
纤维化
内科学
免疫学
生物
血小板
生物化学
酶
作者
Yuji Oe,Nobuyuki Takahashi
出处
期刊:Biomedicines
[MDPI AG]
日期:2022-10-28
卷期号:10 (11): 2737-2737
被引量:7
标识
DOI:10.3390/biomedicines10112737
摘要
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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