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Showing 1-30 of 51 results for "I3875" within Papers
Hidehisa Shimizu et al.
American journal of nephrology, 36(2), 184-189 (2012-08-15)
Increased phosphorylation (activation) of signal transducer and activator of transcription 3 (Stat3) on tyrosine 705 leads to renal fibrosis. Indoxyl sulfate, a uremic toxin, induces renal fibrosis through expression of transforming growth factor-β(1) (TGF-β(1)) in proximal tubular cells. The present
Sung-Jun Hwang et al.
Toxicology letters, 220(2), 109-117 (2013-05-04)
Although AhR activation regulates CD4T cell differentiation, how it works has yet to be elucidated. In the present study, using in vitro Th17 differentiation model, we examined effects of AhR activation by indoxyl 3-sulfate (I3S), a uremic toxin, on Th17
Editorial: A missing link? Monocyte activation by uremic toxins in cardiorenal syndrome.
Ehrin J Armstrong et al.
Journal of leukocyte biology, 93(6), 821-823 (2013-06-01)
Hidehisa Shimizu et al.
American journal of physiology. Cell physiology, 304(7), C685-C692 (2013-02-15)
In chronic kidney disease (CKD), indoxyl sulfate, a uremic toxin, accumulates in serum, and the expression of angiotensinogen (AGT) is upregulated in renal proximal tubular cells. The present study aimed to determine the relationship between indoxyl sulfate and the upregulation
Marlon S L Tijink et al.
Biomaterials, 34(32), 7819-7828 (2013-07-24)
In end stage renal disease (ESRD) waste solutes accumulate in body fluid. Removal of protein bound solutes using conventional renal replacement therapies is currently very poor while their accumulation is associated with adverse outcomes in ESRD. Here we investigate the
Jente Boelaert et al.
Analytical and bioanalytical chemistry, 405(6), 1937-1947 (2013-01-12)
Chronic kidney disease (CKD) is a devastating illness characterized by accumulation of uremic retention solutes in the body. The objective of this study was to develop and validate a simple, rapid, and robust UPLC-MS-MS method for simultaneous determination, in serum
Indoxyl sulfate upregulates liver P-glycoprotein expression and activity through aryl hydrocarbon receptor signaling
Machado, et al.
Journal of the American Society of Nephrology, 29, 906-918 (2018)
Indoxyl-sulfate activation of the AhR-NF-$\kappa$B pathway promotes interleukin-6 secretion and the subsequent osteogenic differentiation of human valvular interstitial cells from the aortic valve
Candellier, et al.
Journal of Molecular and Cellular Cardiology, 179, 18-29 (2023)
Anneleen Pletinck et al.
Journal of the American Society of Nephrology : JASN, 24(12), 1981-1994 (2013-09-07)
Leukocyte activation and endothelial damage both contribute to cardiovascular disease, a major cause of morbidity and mortality in CKD. Experimental in vitro data link several protein-bound uremic retention solutes to the modulation of inflammatory stimuli, including endothelium and leukocyte responses
Ippei Watanabe et al.
Circulation journal : official journal of the Japanese Circulation Society, 77(1), 224-230 (2012-10-06)
Indoxyl sulfate (IS) is a uremic toxin that causes renal injury, but little is known about its adverse effects on the cardiovascular system. The aryl hydrocarbon receptor (AhR) is a ligand-activated transcriptional factor that mediates adaptive and toxic responses in
Sang Zhu et al.
Pharmaceutics, 13(6) (2021-07-03)
The toxicological effects of p-cresol have primarily been attributed to its metabolism products; however, very little human data are available in the key organ (i.e., liver) responsible for the generation of these metabolites. Experiments were conducted in HepaRG cells utilizing
Binding affinity and capacity for the uremic toxin indoxyl sulfate
Devine, et al.
Toxins, 6, 416-429 (2014)
Cheng-jui Lin et al.
Archives of medical research, 44(7), 535-541 (2013-09-24)
P-cresyl sulfate (PCS) and indoxyl sulfate (IS) were not only novel but essential factors associated with cardiovascular disease and mortality in patients with chronic kidney disease and hemodialysis. However, little evidence exams the effect in peritoneal dialysis (PD) patients. This
T Takada et al.
Scientific reports, 8(1), 11147-11147 (2018-07-26)
Chronic kidney disease (CKD) patients accumulate uremic toxins in the body, potentially require dialysis, and can eventually develop cardiovascular disease. CKD incidence has increased worldwide, and preventing CKD progression is one of the most important goals in clinical treatment. In
Jingyuan Song et al.
Bioorganic & medicinal chemistry letters, 23(3), 627-629 (2013-01-08)
An indole compound with a strong purple-red color was produced by boiling a solution of indican under acidic conditions and purified by chromatographies on DEAE-650S Toyopearl TSK-gel and silica-gel columns. The purple-red compound purified was identified as indoxyl red, on
Cheng-Jui Lin et al.
The American journal of the medical sciences, 347(5), 370-376 (2013-09-21)
Protein-bound uremic toxins-indoxyl sulfate (IS) and p-cresyl sulfate (PCS)-can not only predict clinical outcomes but also may relate to bone-mineral disorders in patients with chronic kidney disease (CKD). However, the relationship between protein-bound uremic toxins and fibroblast growth factor 23
Chia-Chang Hsu et al.
Clinical and investigative medicine. Medecine clinique et experimentale, 36(1), E42-E49 (2013-02-05)
Indoxyl sulfate (IS) is linked to endothelial damage, NF-κB activation and induced development of atherosclerosis. The purpose of this study was to investigate the relationship between serum IS levels and the severity of coronary artery stenosis. In addition, the relationship
Carel J Pretorius et al.
Clinica chimica acta; international journal of clinical chemistry, 419, 122-126 (2013-02-23)
The uremic toxins indoxyl sulphate (IS) and p-cresyl sulphate (pCS) are absorbed bacterial metabolites of tryptophan and tyrosine respectively and may be predictive of clinical outcome. Long chromatography times, incomplete data on the reference ranges of the free and total
Bummei Sato et al.
The American journal of cardiology, 111(5), 712-716 (2012-12-12)
The prognosis of patients with diastolic heart failure (HF) is as poor as that of patients with systolic HF. Greater chronic kidney disease-associated mortality occurs in patients with left ventricular (LV) diastolic HF than in those with systolic HF. Indoxyl
Ying-Yong Zhao et al.
Journal of proteome research, 12(2), 692-703 (2012-12-12)
Chronic kidney disease (CKD) is becoming a worldwide public health problem. In this study, a kidney metabonomics method based on the ultra performance liquid chromatography/high-sensitivity mass spectrometry with MS(E) data collection technique was undertaken to explore the excretion pattern of
Liesbeth Viaene et al.
American journal of nephrology, 36(6), 497-508 (2012-11-23)
Local production of 1,25-dihydroxyvitamin D (1,25(OH)(2)D) regulated by the CYP27B1 enzyme in monocytes contributes to the immunomodulatory effects of vitamin D. Uremia suppresses renal CYP27B1, but its impact on monocytic CYP27B1 is incompletely understood. The present study aimed to elucidate
Tetsuhiro Tanaka et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 27(10), 4059-4075 (2013-06-25)
Chronic hypoxia in the tubulointerstitium serves as a final common pathway in progressive renal disease. Circumstantial evidence suggests that hypoxia-inducible factor (HIF)-1 in the ischemic tubules may be functionally inhibited in a chronic kidney disease (CKD) milieu. In this study
Cheng-Jui Lin et al.
Atherosclerosis, 225(1), 173-179 (2012-09-18)
p-Cresyl sulfate (PCS) and indoxyl sulfate (IS) have been reported to predict poor clinical outcomes in hemodialysis (HD) patients. However, little is known about the effect of the two toxins on peripheral arterial disease (PAD) and vascular access dysfunction. Our
Hua Li et al.
Journal of chromatography. A, 1583, 80-87 (2018-11-26)
Modified metabolites play important roles in diagnostic monitoring, oxidative response and physiological regulation. Comprehensive analytical methods are greatly needed for improving the coverage of modified metabolites and studying their physiological function. Here, a novel nontargeted profiling method for mapping modified
Hidehisa Shimizu et al.
Life sciences, 92(2), 143-148 (2012-12-04)
Intercellular adhesion molecule 1 (ICAM-1) plays an important role in adhesion of monocytes/macrophages to injured tubulointerstitial tissue. The present study aimed to determine if indoxyl sulfate, a uremic toxin, regulates renal expression of ICAM-1. The effect of indoxyl sulfate on
Yuying Liu et al.
Cancer cell, 33(3), 480-494 (2018-03-14)
Despite the clinical successes fostered by immune checkpoint inhibitors, mechanisms underlying PD-1 upregulation in tumor-infiltrating T cells remain an enigma. Here, we show that tumor-repopulating cells (TRCs) drive PD-1 upregulation in CD8+ T cells through a transcellular kynurenine (Kyn)-aryl hydrocarbon receptor (AhR)
Tino Vollmer et al.
Scientific reports, 9(1), 14525-14525 (2019-10-12)
Identifying the key toxic players within an in-vivo toxic syndrome is crucial to develop targeted therapies. Here, we established a novel method that characterizes the effect of single substances by means of an ex-vivo incubation set-up. We found that primary
Trace Thome et al.
American journal of physiology. Cell physiology, 317(4), C701-C713 (2019-07-11)
Chronic kidney disease (CKD) leads to increased skeletal muscle fatigue, weakness, and atrophy. Previous work has implicated mitochondria within the skeletal muscle as a mediator of muscle dysfunction in CKD; however, the mechanisms underlying mitochondrial dysfunction in CKD are not
Shinichi Saito et al.
Endocrinology, 155(5), 1899-1907 (2014-03-08)
Activation of (pro)renin receptor (PRR) is involved in the progression of chronic kidney disease. However, the role of indoxyl sulfate, a uremic toxin, in the activation of PRR is not clear. The present study aimed to clarify the role of
Biagio Raffaele Di Iorio et al.
Journal of clinical medicine, 8(9) (2019-09-13)
In chronic kidney disease (CKD), the gut-microbiota metabolites indoxyl sulfate (IS) and p-cresyl sulfate (PCS) progressively accumulate due to their high albumin-binding capacity, leading to clinical complications. In a prospective crossover controlled trial, 60 patients with CKD grades 3B-4 (GFR
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