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Pesquisa : D03.633.100.473.393 [Categoria DeCS]
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[PMID]:29195902
[Au] Autor:Zhang H; Chen J; Shen Z; Gu Y; Xu L; Hu J; Zhang X; Ding X
[Ad] Endereço:Department of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China; Shanghai Institute of Kidney and Dialysis, Shanghai, China; Shanghai Key Laboratory of Kidney and Blood Purification, Shanghai, China.
[Ti] Título:Indoxyl sulfate accelerates vascular smooth muscle cell calcification via microRNA-29b dependent regulation of Wnt/ß-catenin signaling.
[So] Source:Toxicol Lett;284:29-36, 2018 Mar 01.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Vascular calcification (VC) is a very common phenomenon in patients with chronic kidney disease(CKD) and it increases the incidence of cardiovascular disease and leads to high mortality in CKD patients. It has been reported that some microRNAs (miRs) play roles in vascular calcification as an epigenetic regulator. Indoxyl sulfate (IS) is a protein-bound uremic toxin which has been proven as one of the major risk factors of cardiovascular disease in CKD. Here we investigated whether microRNA-29b (miR-29b) is involved in IS-induced vascular calcification. We found that vascular miR-29b was down-regulated in radial arteries of patients with end-stage renal disease. Consistently, IS also decreased miR-29b expression in human aortic smooth muscle cells (HASMCs) and potentiated their calcification. MiR-29b mimics significantly suppressed, while miR-29b anti-miR markedly enhanced, IS-induced runt-related transcription factor 2 and osteopontin expression. The expression of Wnt7b/ß-catenin in radial arteries was higher in end stage renal disease than in control group, and IS increased Wnt7b/ß-catenin expression in HASMCs as early as 3days after stimulation. Furthermore, miR-29b mimics potently repressed Wnt7b/ß-catenin protein expression in HASMCs, whereas miR-29b anti-miR increased their expression, indicating miR-29b indeed negatively regulates Wnt7b/ß-catenin signaling. Dickkopf-1 protein, the Wnt/ß-catenin signaling inhibitor, suppressed anti-miR-29b-enhanced HASMCs calcification. Our data thus indicate that miR-29b downregulation and Wnt/ß-catenin signaling activation may be the key mechanism of IS induced vascular calcification in chronic kidney disease.
[Mh] Termos MeSH primário: Indicã/toxicidade
Falência Renal Crônica/metabolismo
MicroRNAs/metabolismo
Músculo Liso Vascular/efeitos dos fármacos
Calcificação Vascular/metabolismo
Proteínas Wnt/metabolismo
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Técnicas de Cultura de Células
Células Cultivadas
Regulação para Baixo
Seres Humanos
Indicã/metabolismo
MicroRNAs/genética
Músculo Liso Vascular/metabolismo
Artéria Radial/efeitos dos fármacos
Artéria Radial/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CTNNB1 protein, human); 0 (MIRN29 microRNA, human); 0 (MicroRNAs); 0 (WNT7B protein, human); 0 (Wnt Proteins); 0 (beta Catenin); N187WK1Y1J (Indican)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171203
[St] Status:MEDLINE


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[PMID]:29016645
[Au] Autor:Eloot S; Van Biesen W; Roels S; Delrue W; Schepers E; Dhondt A; Vanholder R; Glorieux G
[Ad] Endereço:Department of Nephrology, Ghent University Hospital, Gent, Belgium.
[Ti] Título:Spontaneous variability of pre-dialysis concentrations of uremic toxins over time in stable hemodialysis patients.
[So] Source:PLoS One;12(10):e0186010, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND AIM: Numerous outcome studies and interventional trials in hemodialysis (HD) patients are based on uremic toxin concentrations determined at one single or a limited number of time points. The reliability of these studies however entirely depends on how representative these cross-sectional concentrations are. We therefore investigated the variability of predialysis concentrations of uremic toxins over time. METHODS: Prospectively collected predialysis serum samples of the midweek session of week 0, 1, 2, 3, 4, 8, 12, and 16 were analyzed for a panel of uremic toxins in stable chronic HD patients (N = 18) while maintaining dialyzer type and dialysis mode during the study period. RESULTS: Concentrations of the analyzed uremic toxins varied substantially between individuals, but also within stable HD patients (intra-patient variability). For urea, creatinine, beta-2-microglobulin, and some protein-bound uremic toxins, Intra-class Correlation Coefficient (ICC) was higher than 0.7. However, for phosphorus, uric acid, symmetric and asymmetric dimethylarginine, and the protein-bound toxins hippuric acid and indoxyl sulfate, ICC values were below 0.7, implying a concentration variability within the individual patient even exceeding 65% of the observed inter-patient variability. CONCLUSION: Intra-patient variability may affect the interpretation of the association between a single concentration of certain uremic toxins and outcomes. When performing future outcome and interventional studies with uremic toxins other than described here, one should quantify their intra-patient variability and take into account that for solutes with a large intra-patient variability associations could be missed.
[Mh] Termos MeSH primário: Soluções para Hemodiálise/química
Diálise Renal
Insuficiência Renal Crônica/terapia
Toxinas Biológicas/análise
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Análise de Variância
Arginina/análogos & derivados
Arginina/análise
Creatinina/análise
Feminino
Hipuratos/análise
Seres Humanos
Indicã/análise
Masculino
Meia-Idade
Variações Dependentes do Observador
Fósforo/análise
Ureia/análise
Ácido Úrico/análise
Microglobulina-2 beta/análise
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hemodialysis Solutions); 0 (Hippurates); 0 (Toxins, Biological); 0 (beta 2-Microglobulin); 0 (uremia middle molecule toxins); 268B43MJ25 (Uric Acid); 27YLU75U4W (Phosphorus); 49787G1ULV (symmetric dimethylarginine); 63CV1GEK3Y (N,N-dimethylarginine); 8W8T17847W (Urea); 94ZLA3W45F (Arginine); AYI8EX34EU (Creatinine); N187WK1Y1J (Indican); TE0865N2ET (hippuric acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171011
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186010


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[PMID]:28791957
[Au] Autor:Kaminski T; Michalowska M; Pawlak D
[Ad] Endereço:Zaklad Farmakodynamiki, Uniwersytet Medyczny w Bialymstoku.
[Ti] Título:Aryl hydrocarbon receptor (AhR) and its endogenous agonist - indoxyl sulfate in chronic kidney disease.
[So] Source:Postepy Hig Med Dosw (Online);71(0):624-632, 2017 Jul 30.
[Is] ISSN:1732-2693
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:The indoxyl sulfate (IS, indoxyl sulphate) is the end product of dietary tryptophan degradation by indole pathway and significantly higher serum and tissue concentrations of this compound is observed in patients with impaired renal function. Despite the high albumin binding affinity, the remaining free fraction of IS has a number of biological effects related to the generation of oxidative stress andactivation of signaling pathways related to NF-кB, p53 protein, STAT3, TGF-ß and Smad2/3. IS induces the inflammatory process, exerts nephrotoxic activity and is also a factor impairing the cardiovascular system.Its high concentrations are associated with the occurrence of cardiovascular incidents, whose frequency is significantly higher in patients with chronic kidney disease. Evaluation of the mechanisms that underlie the high reactivity of indoxyl sulfate and its biological effects showed that this compound is an agonist of the aryl hydrocarbon receptor (AhR). This receptor plays an important role in maintaining homeostasis Moreover, AhR exerts high transcriptional activity, so ligands of obciazethis receptor may exert different biological effects. The following paper describes the role of indoxyl sulfate as AhR ligand in the context of the excessive accumulation, which appears as one of the symptoms associated with chronic kidney disease.
[Mh] Termos MeSH primário: Indicã/farmacologia
Receptores de Hidrocarboneto Arílico/agonistas
Insuficiência Renal Crônica/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Indicã/toxicidade
Insuficiência Renal Crônica/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Receptors, Aryl Hydrocarbon); N187WK1Y1J (Indican)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE


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[PMID]:28754616
[Au] Autor:Gao H; Liu S
[Ad] Endereço:School of Medicine, South China University of Technology, Guangzhou 510006, China.
[Ti] Título:Role of uremic toxin indoxyl sulfate in the progression of cardiovascular disease.
[So] Source:Life Sci;185:23-29, 2017 Sep 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The prevalence of cardiovascular disease (CVD) among patients with chronic kidney disease (CKD) is relatively high. Deterioration of renal function in CKD leads to accumulation of indoxyl sulfate, a tryptophan metabolite produced by gut microbiota. It is acknowledged that indoxyl sulfate is capable to stimulate oxidative stress, which in turn contributes to the progression of vascular disorders and its resultant coronary artery disease. Recent research have demonstrated the adverse effects of indoxyl sulfate on the heart, together with the acceleration of vascular dysfunction, suggesting that indoxyl sulfate might contribute to high prevalence of CVD in CKD. The present mini review has focused on the potential mechanisms by which indoxyl sulfate exerts this pro-oxidant effects on the cardiovascular system. The action of indoxyl sulfate are related to multiple NADPH oxidase-mediated redox signaling pathways, which have been implicated in the pathophysiology of different forms of CVD, including chronic heart failure, arrhythmia, atherosclerotic vascular disease and coronary calcification. Future therapeutic options are discussed, including modulating gut microbial flora and blocking responsible pathophysiologic pathways.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/fisiopatologia
Indicã/metabolismo
Insuficiência Renal Crônica/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Doença da Artéria Coronariana/fisiopatologia
Progressão da Doença
Seres Humanos
NADPH Oxidases/metabolismo
Oxirredução
Estresse Oxidativo/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
EC 1.6.3.- (NADPH Oxidases); N187WK1Y1J (Indican)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170730
[St] Status:MEDLINE


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[PMID]:28528271
[Au] Autor:Deltombe O; de Loor H; Glorieux G; Dhondt A; Van Biesen W; Meijers B; Eloot S
[Ad] Endereço:Renal Division - Ghent University Hospital, De Pintelaan 185, 9000, Ghent, Belgium. Electronic address: Olivier.Deltombe@UGent.be.
[Ti] Título:Exploring binding characteristics and the related competition of different protein-bound uremic toxins.
[So] Source:Biochimie;139:20-26, 2017 Aug.
[Is] ISSN:1638-6183
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Little is known about potential differences in binding characteristics of protein-bound uremic toxins (PBUTs) in patients with chronic kidney disease (CKD) versus healthy controls. The question arises whether eventual differences are attributed to (i) the elevated levels of competing uremic toxins, and/or (ii) post-translational modifications of albumin. We evaluated the binding characteristics of hippuric acid (HA), indole-3-acetic acid (IAA), indoxyl sulfate (IS), and p-cresylsulfate (pCS) by deriving a binding curve in three distinct conditions: (i) serum from healthy controls (healthy serum), (ii) blank serum from hemodialysis patients (blank HD serum; i.e. cleared from uremic toxins), and (iii) non-treated serum from HD patients (HD serum). Additionally, the mutual binding competition of these uremic toxins was studied in blank HD in pairs. In both experiments, equilibrium dialysis (37 °C, 5 h) was used to separate the free and bound fractions of each PBUT. Free and total PBUT concentrations were quantified by an ultra-high performance liquid chromatography method with tandem mass spectrometer detection and the percentage protein binding (%PB) of each PBUT was calculated. For all four compounds, the binding capacity of healthy serum was higher than blank HD serum, which was comparable to non-treated HD serum, except for HA. The competition experiments revealed that at high uremic concentrations, mutual competition was observed for the strongly bound PBUTs IS and pCS. The %PB of the weakly bound HA and IAA was lower (trend) only for the addition to blank HD serum containing the strongly bound IS or pCS. There is an intrinsic impact on protein binding in uremia, revealing a lower binding capacity, as compared to healthy controls. Competitive binding is only relevant for the strongly bound PBUTs at high uremic concentrations. In addition, at least part of the effect on binding capacity can be attributed to post-translational modifications of albumin.
[Mh] Termos MeSH primário: Diálise Renal
Insuficiência Renal Crônica/metabolismo
Albumina Sérica/metabolismo
Toxinas Biológicas/metabolismo
Uremia/fisiopatologia
[Mh] Termos MeSH secundário: Ligação Competitiva
Estudos de Casos e Controles
Cromatografia Líquida de Alta Pressão
Cresóis/metabolismo
Hipuratos/metabolismo
Seres Humanos
Indicã/metabolismo
Ácidos Indolacéticos/metabolismo
Ligação Proteica
Processamento de Proteína Pós-Traducional
Insuficiência Renal Crônica/terapia
Ésteres do Ácido Sulfúrico/metabolismo
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cresols); 0 (Hippurates); 0 (Indoleacetic Acids); 0 (Serum Albumin); 0 (Sulfuric Acid Esters); 0 (Toxins, Biological); 56M34ZQY1S (4-cresol sulfate); 6U1S09C61L (indoleacetic acid); N187WK1Y1J (Indican); TE0865N2ET (hippuric acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170522
[St] Status:MEDLINE


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[PMID]:28472795
[Au] Autor:Favretto G; Souza LM; Gregório PC; Cunha RS; Maciel RAP; Sassaki GL; Toledo MG; Pecoits-Filho R; Souza WM; Stinghen AEM
[Ad] Endereço:Experimental Nephrology Laboratory, Basic Pathology Department, Universidade Federal do Paraná, Curitiba, Brazil.
[Ti] Título:Role of Organic Anion Transporters in the Uptake of Protein-Bound Uremic Toxins by Human Endothelial Cells and Monocyte Chemoattractant Protein-1 Expression.
[So] Source:J Vasc Res;54(3):170-179, 2017.
[Is] ISSN:1423-0135
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Organic anion transporters (OATs) are involved in the uptake of uremic toxins such as p-cresyl sulfate (PCS) and indoxyl sulfate (IS), which play a role in endothelial dysfunction in patients with chronic kidney diseases (CKD). In this study, we investigated the role of OAT1 and OAT3 in the uptake of PCS and IS into human endothelial cells. PCS was synthesized via p-cresol sulfation and characterized using analytical methods. The cells were treated with PCS and IS in the absence and presence of probenecid (Pb), an OAT inhibitor. Cell viability was assessed using the MTT assay. The absorbed toxins were analyzed using chromatography, OAT expression using immunocytochemistry and western blot, and monocyte chemoattractant protein-1 (MCP-1) expression using enzyme-linked immunosorbent assay. Cell viability decreased after toxin treatment in a dose-dependent manner. PCS and IS showed significant internalization after 60 min treatment, while no internalization was observed in the presence of Pb, suggesting that OATs are involved in the transport of both toxins. Immunocytochemistry and western blot demonstrated OAT1 and OAT3 expression in endothelial cells. MCP-1 expression increased after toxins treatment but decreased after Pb treatment. PCS and IS uptake were mediated by OATs, and OAT blockage could serve as a therapeutic strategy to inhibit MCP-1 expression.
[Mh] Termos MeSH primário: Quimiocina CCL2/metabolismo
Células Endoteliais/metabolismo
Proteína 1 Transportadora de Ânions Orgânicos/metabolismo
Transportadores de Ânions Orgânicos Sódio-Independentes/metabolismo
Uremia/metabolismo
[Mh] Termos MeSH secundário: Transporte Biológico
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Cresóis/metabolismo
Cresóis/toxicidade
Relação Dose-Resposta a Droga
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/patologia
Seres Humanos
Indicã/metabolismo
Indicã/toxicidade
Proteína 1 Transportadora de Ânions Orgânicos/antagonistas & inibidores
Transportadores de Ânions Orgânicos Sódio-Independentes/antagonistas & inibidores
Probenecid/farmacologia
Ésteres do Ácido Sulfúrico/metabolismo
Ésteres do Ácido Sulfúrico/toxicidade
Fatores de Tempo
Regulação para Cima
Uremia/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCL2 protein, human); 0 (Chemokine CCL2); 0 (Cresols); 0 (Organic Anion Transport Protein 1); 0 (Organic Anion Transporters, Sodium-Independent); 0 (Sulfuric Acid Esters); 0 (organic anion transport protein 3); 56M34ZQY1S (4-cresol sulfate); N187WK1Y1J (Indican); PO572Z7917 (Probenecid)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1159/000468542


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[PMID]:28445490
[Au] Autor:Ali BH; Karaca T; Al Suleimani Y; Al Za'abi M; Al Kalbani J; Ashique M; Nemmar A
[Ad] Endereço:Department of Pharmacology and Clinical Pharmacy, College of Medicine and Health Sciences, Sultan Qaboos University, Al Khod, Oman.
[Ti] Título:The effect of swimming exercise on adenine-induced kidney disease in rats, and the influence of curcumin or lisinopril thereon.
[So] Source:PLoS One;12(4):e0176316, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Patients with chronic kidney disease (CKD) have been reported to benefit from different types of exercises. It has also been shown that the ACE inhibitor lisinopril, and the natural product curcumin are also beneficial in different models of CKD in rats. We assessed the influence of moderate swimming exercise (SE) on rats with adenine-induced CKD, and tested the possible effects of lisinopril and/or curcumin thereon using several physiological, biochemical, histopathological and immunohistochemical parameters. Rats (either sedentary or subjected to SE) were randomly divided into several groups, and given for five weeks either normal food or food mixed with adenine (0.25% w/w) to induce CKD. Some of these groups were also concomitantly treated orally with curcumin (75 mg/kg), or lisinopril (10 mg/kg) and were subjected to moderate SE (45 min/day three days each week). Rats fed adenine showed the typical biochemical, histopathological signs of CKD such as elevations in blood pressure, urinary albumin / creatinine ratio, and plasma urea, creatinine, indoxyl sulfate and phosphorus. SE, curcumin or lisinopril, given singly, significantly ameliorated all the adenine-induced actions. Administering curcumin or lisinopril with SE improved the histopathology of the kidneys, a salutary effect not seen with SE alone. Combining SE to the nephroprotective agents' curcumin or lisinopril might offer additional nephroprotection.
[Mh] Termos MeSH primário: Curcumina
Rim/efeitos dos fármacos
Lisinopril
Substâncias Protetoras
Insuficiência Renal Crônica/tratamento farmacológico
Natação
[Mh] Termos MeSH secundário: Adenina/toxicidade
Animais
Antioxidantes/metabolismo
Pressão Sanguínea/efeitos dos fármacos
Creatinina/sangue
Creatinina/urina
Curcumina/farmacologia
Curcumina/uso terapêutico
Modelos Animais de Doenças
Feminino
Imuno-Histoquímica
Indicã/sangue
Rim/metabolismo
Rim/patologia
Lisinopril/farmacologia
Lisinopril/uso terapêutico
Condicionamento Físico Animal
Substâncias Protetoras/farmacologia
Substâncias Protetoras/uso terapêutico
Ratos
Ratos Sprague-Dawley
Insuficiência Renal Crônica/induzido quimicamente
Insuficiência Renal Crônica/patologia
Albumina Sérica/análise
Ureia/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Protective Agents); 0 (Serum Albumin); 8W8T17847W (Urea); AYI8EX34EU (Creatinine); E7199S1YWR (Lisinopril); IT942ZTH98 (Curcumin); JAC85A2161 (Adenine); N187WK1Y1J (Indican)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0176316


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[PMID]:28420181
[Au] Autor:Barreto FC; Barreto DV; Stinghen AEM; Massy ZA
[Ad] Endereço:Division of Nephrology, Department of Internal Medicine, Federal University of Paraná, 80060-900 Curitiba, Brazil. fellype.barreto@ufpr.br.
[Ti] Título:Comment on Indoxyl Sulfate-Review of Toxicity and Therapeutic Strategies. Toxins 2016, 8, 358.
[So] Source:Toxins (Basel);9(4), 2017 04 17.
[Is] ISSN:2072-6651
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Recently, the clinical and experimental evidences that support the toxic effects of indoxyl sulfate, a protein-bound uremic toxin in chronic kidney disease (CKD) patients, has been discussed. In this panorama, the authors described several in vitro and in vivo studies, suggesting that indoxyl sulfate may play a part in the pathogenesis of low turnover bone disease. However, the discussion claims the need for relevant clinical studies in CKD patients whose bone turnover biomarkers and bone histomorphometry were assessed in order to demonstrate the association between serum levels of indoxyl sulfate and bone turnover. We would like to underline the availability of this clinical data to support the concept that indoxyl sulfate may play a part in the pathogenesis of low turnover bone disease in CKD patients.
[Mh] Termos MeSH primário: Indicã/sangue
Toxinas Biológicas/sangue
[Mh] Termos MeSH secundário: Biomarcadores
Seres Humanos
Insuficiência Renal Crônica
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (Biomarkers); 0 (Toxins, Biological); N187WK1Y1J (Indican)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170420
[St] Status:MEDLINE


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[PMID]:28277985
[Au] Autor:Chu S; Mao X; Guo H; Wang L; Li Z; Zhang Y; Wang Y; Wang H; Zhang X; Peng W
[Ad] Endereço:a Laboratory of Renal Disease , Putuo Hospital, Shanghai University of Traditional Chinese Medicine , Shanghai , China.
[Ti] Título:Indoxyl sulfate potentiates endothelial dysfunction via reciprocal role for reactive oxygen species and RhoA/ROCK signaling in 5/6 nephrectomized rats.
[So] Source:Free Radic Res;51(3):237-252, 2017 Mar.
[Is] ISSN:1029-2470
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Accumulative indoxyl sulfate (IS) retained in chronic kidney disease (CKD) can potentiate vascular endothelial dysfunction, and herein, we aim at elucidating the underlying mechanisms from the perspective of possible association between reactive oxygen species (ROS) and RhoA/ROCK pathway. IS-treated nephrectomized rats are administered with antioxidants including NADPH oxidase inhibitor apocynin, SOD analog tempol, and mitochondrion-targeted SOD mimetic mito-TEMPO to scavenge ROS, or ROCK inhibitor fasudil to obstruct RhoA/ROCK pathway. First, we find in response to IS stimulation, antioxidants treatments suppress increased aortic ROCK activity and expression levels. Additionally, ROCK blockade prevent IS-induced increased NADPH oxidase expression (mainly p22phox and p47phox), mitochondrial and intracellular ROS (superoxide and hydrogen peroxide) generation, and decreased Cu/Zn-SOD expression in thoracic aortas. Apocynin, mito-TEMPO, and tempol also reverse these markers of oxidative stress. These results suggest that IS induces excessive ROS production and ROCK activation involving a circuitous relationship in which ROS activate ROCK and ROCK promotes ROS overproduction. Finally, ROS and ROCK depletion attenuate IS-induced decrease in nitric oxide (NO) production and eNOS expression levels, and alleviate impaired vasomotor responses including increased vasocontraction to phenylephrine and decreased vasorelaxation to acetylcholine, thereby preventing cardiovascular complications accompanied by CKD. Taken together, excessive ROS derived from NADPH oxidase and mitochondria coordinate with RhoA/ROCK activation in a form of positive reciprocal relationship to induce endothelial dysfunction through disturbing endothelium-dependent NO signaling upon IS stimulation in CKD status.
[Mh] Termos MeSH primário: Antioxidantes/administração & dosagem
Estresse Oxidativo/efeitos dos fármacos
Insuficiência Renal Crônica/tratamento farmacológico
Proteínas rho de Ligação ao GTP/metabolismo
Quinases Associadas a rho/metabolismo
[Mh] Termos MeSH secundário: 1-(5-Isoquinolinasulfonil)-2-Metilpiperazina/administração & dosagem
1-(5-Isoquinolinasulfonil)-2-Metilpiperazina/análogos & derivados
Acetofenonas/administração & dosagem
Animais
Óxidos N-Cíclicos/administração & dosagem
Endotélio Vascular/efeitos dos fármacos
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Indicã/toxicidade
NADPH Oxidases/metabolismo
Óxido Nítrico/biossíntese
Óxido Nítrico Sintase Tipo III/biossíntese
Compostos Organofosforados/administração & dosagem
Piperidinas/administração & dosagem
Ratos
Espécies Reativas de Oxigênio/metabolismo
Insuficiência Renal Crônica/induzido quimicamente
Insuficiência Renal Crônica/metabolismo
Transdução de Sinais/efeitos dos fármacos
Marcadores de Spin
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetophenones); 0 (Antioxidants); 0 (Cyclic N-Oxides); 0 (MitoTEMPO); 0 (Organophosphorus Compounds); 0 (Piperidines); 0 (Reactive Oxygen Species); 0 (Spin Labels); 31C4KY9ESH (Nitric Oxide); 84477-87-2 (1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine); B6J7B9UDTR (acetovanillone); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 1.14.13.39 (Nos3 protein, rat); EC 1.6.3.- (NADPH Oxidases); EC 2.7.11.1 (rho-Associated Kinases); EC 3.6.5.2 (RhoA protein, rat); EC 3.6.5.2 (rho GTP-Binding Proteins); N187WK1Y1J (Indican); Q0CH43PGXS (fasudil); U78ZX2F65X (tempol)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1080/10715762.2017.1296575


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[PMID]:28264799
[Au] Autor:Yang K; Du C; Wang X; Li F; Xu Y; Wang S; Chen S; Chen F; Shen M; Chen M; Hu M; He T; Su Y; Wang J; Zhao J
[Ad] Endereço:Department of Nephrology, Xinqiao Hospital, Third Military Medical University, Chongqing, China; and.
[Ti] Título:Indoxyl sulfate induces platelet hyperactivity and contributes to chronic kidney disease-associated thrombosis in mice.
[So] Source:Blood;129(19):2667-2679, 2017 May 11.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thrombosis is a common complication of chronic kidney disease (CKD), but the causes and mechanisms of CKD-associated thrombosis are not well clarified. Here, we show that platelet activity is remarkably enhanced in CKD mice, with increase of serum indoxyl sulfate (IS), a typical uremic toxin, which cannot be effectively cleared by routine dialysis. Ex vivo and in vitro experiments reveal that IS displays a distinct ability to enhance platelet activities, including elevated response to collagen and thrombin, increases in platelet-derived microparticles, and platelet-monocyte aggregates. The flow chamber assay and carotid artery thrombosis model demonstrate that IS-induced platelet hyperactivity contributes to thrombus formation. Further investigations disclose that reactive oxygen species (ROS)-mediated p38MAPK signaling plays a key role in IS-induced platelet hyperactivity. Moreover, we show that Klotho, which is expressed dominantly in the kidneys, has the capacity to counteract IS-induced platelet hyperactivity by inhibiting ROS/p38MAPK signaling, whereas Klotho reduction may aggravate the effect of IS on platelet activation in CKD and mice. Finally, we demonstrate that Klotho protein treatment can protect against IS-induced thrombosis and atherosclerosis in mice. Our findings uncover the mechanism of platelet hyperactivity induced by IS and provide new insights into the pathogenesis and treatment of CKD-associated thrombosis.
[Mh] Termos MeSH primário: Plaquetas/efeitos dos fármacos
Indicã/efeitos adversos
Ativação Plaquetária/efeitos dos fármacos
Insuficiência Renal Crônica/induzido quimicamente
Trombose/induzido quimicamente
[Mh] Termos MeSH secundário: Animais
Plaquetas/patologia
Glucuronidase/administração & dosagem
Glucuronidase/metabolismo
Glucuronidase/uso terapêutico
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Espécies Reativas de Oxigênio/metabolismo
Insuficiência Renal Crônica/metabolismo
Trombose/tratamento farmacológico
Trombose/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Reactive Oxygen Species); EC 3.2.1.31 (Glucuronidase); EC 3.2.1.31 (klotho protein); N187WK1Y1J (Indican)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170308
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2016-10-744060



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