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Tissue Factor, Thrombosis, and Chronic Kidney Disease

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 al...

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Autores principales: Oe, Yuji, Takahashi, Nobuyuki
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9687479/
https://www.ncbi.nlm.nih.gov/pubmed/36359257
http://dx.doi.org/10.3390/biomedicines10112737
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author Oe, Yuji
Takahashi, Nobuyuki
author_facet Oe, Yuji
Takahashi, Nobuyuki
author_sort Oe, Yuji
collection PubMed
description 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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spelling pubmed-96874792022-11-25 Tissue Factor, Thrombosis, and Chronic Kidney Disease Oe, Yuji Takahashi, Nobuyuki Biomedicines Review 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. MDPI 2022-10-28 /pmc/articles/PMC9687479/ /pubmed/36359257 http://dx.doi.org/10.3390/biomedicines10112737 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Oe, Yuji
Takahashi, Nobuyuki
Tissue Factor, Thrombosis, and Chronic Kidney Disease
title Tissue Factor, Thrombosis, and Chronic Kidney Disease
title_full Tissue Factor, Thrombosis, and Chronic Kidney Disease
title_fullStr Tissue Factor, Thrombosis, and Chronic Kidney Disease
title_full_unstemmed Tissue Factor, Thrombosis, and Chronic Kidney Disease
title_short Tissue Factor, Thrombosis, and Chronic Kidney Disease
title_sort tissue factor, thrombosis, and chronic kidney disease
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9687479/
https://www.ncbi.nlm.nih.gov/pubmed/36359257
http://dx.doi.org/10.3390/biomedicines10112737
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