scholarly journals Aryl Hydrocarbon Receptor Activation in Chronic Kidney Disease: Role of Uremic Toxins

Nephron ◽  
2017 ◽  
Vol 137 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Jessyca S. Brito ◽  
Natália A. Borges ◽  
Marta Esgalhado ◽  
D''Angelo C. Magliano ◽  
Christophe O. Soulage ◽  
...  
2020 ◽  
Vol 177 (15) ◽  
pp. 3415-3435 ◽  
Author(s):  
Hua Miao ◽  
Gang Cao ◽  
Xia‐Qing Wu ◽  
Yuan‐Yuan Chen ◽  
Dan‐Qian Chen ◽  
...  

Biochemistry ◽  
2019 ◽  
Vol 58 (15) ◽  
pp. 2054-2060 ◽  
Author(s):  
Jessyca Sousa de Brito ◽  
Natália Alvarenga Borges ◽  
Juliana Saraiva dos Anjos ◽  
Lia Sumie Nakao ◽  
Milena Barcza Stockler-Pinto ◽  
...  

2021 ◽  
Vol 22 (19) ◽  
pp. 10549
Author(s):  
Ophélie Fourdinier ◽  
Griet Glorieux ◽  
Benjamin Brigant ◽  
Momar Diouf ◽  
Anneleen Pletinck ◽  
...  

Chronic kidney disease (CKD) is a major cause of death worldwide and is associated with a high risk for cardiovascular and all-cause mortality. In CKD, endothelial dysfunction occurs and uremic toxins accumulate in the blood. miR-126 is a regulator of endothelial dysfunction and its blood level is decreased in CKD patients. In order to obtain a better understanding of the physiopathology of the disease, we correlated the levels of miR-126 with several markers of endothelial dysfunction, as well as the representative uremic toxins, in a large cohort of CKD patients at all stages of the disease. Using a univariate analysis, we found a correlation between eGFR and most markers of endothelial dysfunction markers evaluated in this study. An association of miR-126 with all the evaluated uremic toxins was also found, while uremic toxins were not associated with the internal control, specifically cel-miR-39. The correlation between the expression of endothelial dysfunction biomarker Syndecan-1, free indoxyl sulfate, and total p-cresyl glucuronide on one side, and miR-126 on the other side was confirmed using multivariate analysis. As CKD is associated with reduced endothelial glycocalyx (eGC), our results justify further evaluation of the role of correlated parameters in the pathophysiology of CKD.


2017 ◽  
Vol 27 (5) ◽  
pp. 359 ◽  
Author(s):  
P. V. L. N.Srinivasa Rao ◽  
S Gouroju ◽  
AR Bitla ◽  
KS Vinapamula ◽  
SM Manohar ◽  
...  

Toxins ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 412 ◽  
Author(s):  
Tawfik Addi ◽  
Laetitia Dou ◽  
Stéphane Burtey

Patients with chronic kidney disease (CKD) display an elevated risk of thrombosis. Thrombosis occurs in cardiovascular events, such as venous thromboembolism, stroke, and acute coronary syndrome, and is a cause of hemodialysis vascular access dysfunction. CKD leads to the accumulation of uremic toxins, which exerts toxic effects on blood and the vessel wall. Some uremic toxins result from tryptophan metabolization in the gut through the indolic and the kynurenine pathways. An increasing number of studies are highlighting the link between such uremic toxins and thrombosis in CKD. In this review, we describe the thrombotic mechanisms induced by tryptophan-derived uremic toxins (TDUT). These mechanisms include an increase in plasma levels of procoagulant factors, induction of platelet hyperactivity, induction of endothelial dysfunction/ impairment of endothelial healing, decrease in nitric oxide (NO) bioavailability, and production of procoagulant microparticles. We focus on one important prothrombotic mechanism: The induction of tissue factor (TF), the initiator of the extrinsic pathway of the blood coagulation. This induction occurs via a new pathway, dependent on the transcription factor Aryl hydrocarbon receptor (AhR), the receptor of TDUT in cells. A better understanding of the prothrombotic mechanisms of uremic toxins could help to find novel therapeutic targets to prevent thrombosis in CKD.


2012 ◽  
Vol 22 (1) ◽  
pp. 98-101 ◽  
Author(s):  
Hisae Tanaka ◽  
Hirotaka Komaba ◽  
Masahiro Koizumi ◽  
Takatoshi Kakuta ◽  
Masafumi Fukagawa

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Hui Zhao ◽  
Lin Chen ◽  
Tian Yang ◽  
Ya-Long Feng ◽  
Nosratola D. Vaziri ◽  
...  

2018 ◽  
Vol 93 (4) ◽  
pp. 986-999 ◽  
Author(s):  
Laetitia Dou ◽  
Stéphane Poitevin ◽  
Marion Sallée ◽  
Tawfik Addi ◽  
Bertrand Gondouin ◽  
...  

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