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Condition: Renal Failure

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Total 60 results found since Jan 2013.

Puerarin improves methotrexate-induced renal damage by up-regulating renal expression of Oat1 and Oat3 in vivo and in vitro
Publication date: July 2018 Source:Biomedicine & Pharmacotherapy, Volume 103 Author(s): Qi Liu, Zhihao Liu, Xiaokui Huo, Changyuan Wang, Qiang Meng, Huijun Sun, Pengyuan Sun, Jinyong Peng, Xiaodong Ma, Kexin Liu The regulation of renal transporters such as organic anion transporter (OATs) is a new target for treatment of acute renal failure. The purpose of this study was to investigate whether the effect of puerarin (Pur) on renal damage induced by methotrexate (MTX) is related to the expression of renal Oat1/3 in vivo and in vitro, and to explore the related mechanisms. Effect of Pur on the renal damage caused by...
Source: Biomedicine and Pharmacotherapy - April 25, 2018 Category: Drugs & Pharmacology Source Type: research

Protective effect of Gelofusine against cRGD-siRNA-induced nephrotoxicity in mice.
Authors: Liao W, Qin Y, Liao L, Cen B, Wu Z, Wei Y, Wang Z, Li G, Ji A Abstract Based on successful targeting to the αvβ3 integrin of cyclic arginine-glycine-aspartic acid (cRGD), cRGD-conjugated small interfering RNA (siRNA) exhibits tumor targeting and has become a new treatment strategy for solid tumors. However, the nephrotoxicity caused by its renal retention limits its clinical application. Here, we evaluated the protective effect of Gelofusine against cRGD-conjugated siRNA-induced nephrotoxicity in mice. Male Kunming mice (six per group) were either co-injected with Gelofusine and cRGD-siRNA or injected wi...
Source: Renal Failure - April 7, 2018 Category: Urology & Nephrology Tags: Ren Fail Source Type: research

FTY720 ameliorates renal fibrosis by simultaneously affecting leucocyte recruitment and TGF ‐β signalling in fibroblasts
In this study, we evaluated the effect of fingolimod (FTY720), an analogue of sphingosine 1‐phosphate (S1P), as a treatment for the unilateral ureteral obstruction (UUO)‐induced renal fibrosis animal model. We treated mice with FTY720 at a dosage of 1 mg/kg/day by intragastric administration from day 1 until day 7. The control group received the same amount of saline. FTY720 reduced significantly the urine albumin/creatinine ratio (UACR) in treated UUO mice. FTY720 treatment also caused a significant decrease in interstitial expansion and collagen deposition in the kidney, accompanied by reduced mononuclear cell recrui...
Source: Clinical and Experimental Immunology - July 27, 2017 Category: Allergy & Immunology Authors: T. Tian, J. Zhang, X. Zhu, S. Wen, D. Shi, H. Zhou Tags: Original Article Source Type: research

FTY720 ameliorates renal fibrosis by simultaneously affecting leukocyte recruitment and TGF ‐β signaling in fibroblasts
This article is protected by copyright. All rights reserved.
Source: Clinical and Experimental Immunology - June 28, 2017 Category: Allergy & Immunology Authors: Tongguan Tian, Jun Zhang, Xingxing Zhu, Shuang Wen, Dongyan Shi, Hong Zhou Tags: Original Article Source Type: research

FTY720 ameliorates renal fibrosis by simultaneously affecting leukocyte recruitment and TGF- β signaling in fibroblasts.
This article is protected by copyright. All rights reserved. PMID: 28658504 [PubMed - as supplied by publisher]
Source: Clinical and Developmental Immunology - June 28, 2017 Category: Allergy & Immunology Authors: Tian T, Zhang J, Zhu X, Wen S, Shi D, Zhou H Tags: Clin Exp Immunol Source Type: research

TMEM16A exacerbates renal injury by activating P38/JNK signaling pathway to promote podocyte apoptosis in diabetic nephropathy mice.
Abstract Diabetic nephropathy (DN) is one of the most common microvascular complication of diabetes mellitus (DM) as well as the main reason resulting in chronic renal failure. Transmembrane protein 16A (TMEM16A) plays an important role in multiple physiological actions. Here we found that it was up-regulated in high-fat diet (HFD)/streptozotocin (STZ)-induced diabetic mice. Moreover, reverse transcription-polymerase chain reaction (RT-PCR) amplification, Western blot detection, Periodic Acid Schiff (PAS) staining and immunohistochemical analysis confirmed that TMEM16A deficiency alleviated renal injury in diabeti...
Source: Biochemical and Biophysical Research communications - April 6, 2017 Category: Biochemistry Authors: Lian H, Cheng Y, Wu X Tags: Biochem Biophys Res Commun Source Type: research

STAT5 drives abnormal proliferation in autosomal dominant polycystic kidney disease
Autosomal dominant polycystic kidney disease (ADPKD) leads to renal failure. The hallmark of ADPKD is increased epithelial proliferation, which has been proposed to be due to atypical signaling including abnormal JAK-STAT activity. However, the relative contribution of JAK-STAT family members in promoting proliferation in ADPKD is unknown. Here, we present siRNA JAK-STAT –focused screens discovering a previously unknown proliferative role for multiple JAK-STAT components (including STAT1, STAT2, STAT4, STAT5a, and STAT5b).
Source: Kidney International - January 15, 2017 Category: Urology & Nephrology Authors: Maria Fragiadaki, Morgane Lannoy, Madeleine Themanns, Barbara Maurer, Wouter N. Leonhard, Dorien J.M. Peters, Richard Moriggl, Albert C.M. Ong Tags: Basic Research Source Type: research

Renin-angiotensin system activation accelerates atherosclerosis in experimental renal failure by promoting endoplasmic reticulum stress-related inflammation.
In this study, we investigated the association between the renin-angiotensin system (RAS), endoplasmic reticulum (ER) stress and atherosclerosis (AS) in uremic apolipoprotein E knockout (apoE-/-) mice. Mild uremia was induced by a 5/6 nephrectomy (5/6 Nx) in 10-week-old apoE-/- mice. Four weeks after nephrectomy, the mice received losartan or no treatment for 16 weeks. Sham-operated mice served as the controls. We found that uremia accelerated AS at the aortic root. The activation of ER stress and the significant upregulation of pro-inflammatory cytokines and chemokines were observed in the uremic mice. Phosphoryla...
Source: International Journal of Molecular Medicine - January 11, 2017 Category: Molecular Biology Authors: Yang J, Zhang X, Yu X, Tang W, Gan H Tags: Int J Mol Med Source Type: research

Decrease in acrolein toxicity based on the decline of polyamine oxidases.
Abstract We have shown recently that acrolein is strongly involved in cell damage during brain infarction and chronic renal failure. To study the mechanism of acrolein detoxification, we tried to isolate Neuro2a cells with reduced sensitivity to acrolein toxicity (Neuro2a-ATD cells). In one cell line, Neuro2a-ATD1, the level of glutathione (GSH) was increased. We recently isolated a second cell line, Neuro2a-ATD2, and found that acrolein-producing enzymes [polyamine oxidases (PAO); i.e. acetylpolyamine oxidase (AcPAO), and spermine oxidase (SMO)] are reduced in this cell line due to changes at the level of transcr...
Source: The International Journal of Biochemistry and Cell Biology - August 29, 2016 Category: Biochemistry Authors: Uemura T, Nakamura M, Sakamoto A, Suzuki T, Dohmae N, Terui Y, Tomitori H, Casero RA, Kashiwagi K, Igarashi K Tags: Int J Biochem Cell Biol Source Type: research

Calcineurin Inhibitors Downregulate HNF-1β and May Affect the Outcome of HNF1B Patients After Renal Transplantation
Conclusions: Because HNF1B-related disease is a heterozygous condition, CNIs used to prevent rejection may induce reduced expression of the nonmutated allele of HNF1B leading to a superimposed defect of HNF-1β transcriptional activity. Taking into account the specific risk of posttransplantation diabetes mellitus and liver disorders in HNF1B patients, these findings advocate for in-depth characterization of pathways that regulate HNF1B and plead for considering individually tailored graft management that may include a CNI-free immunosuppressive regimen. Interventional studies will have to confirm this individualized approach.
Source: Transplantation - August 24, 2016 Category: Transplant Surgery Tags: Original Clinical Science-General Source Type: research

Reactive oxygen species are involved in insulin-dependent regulation of autophagy in primary rat podocytes.
Abstract Autophagy is an intracellular defense mechanism responsible for the turnover of damaged or non-functional cellular constituents. This process provides cells with energy and essential compounds under unfavorable environmental conditions-such as oxidative stress and hyperglycemia, which are both observed in diabetes. The most common diabetes complication is diabetic nephropathy (DN), which can lead to renal failure. This condition often includes impaired podocyte function. Here we investigated autophagic activity in rat podocytes cultured with a high insulin concentration (300nM). Autophagy was activated af...
Source: The International Journal of Biochemistry and Cell Biology - March 25, 2016 Category: Biochemistry Authors: Audzeyenka I, Rogacka D, Piwkowska A, Rychlowski M, Bierla JB, Czarnowska E, Angielski S, Jankowski M Tags: Int J Biochem Cell Biol Source Type: research

Metabolism of 13C5-hydroxyproline in mouse models of primary hyperoxaluria and its inhibition by RNAi therapeutics targeting liver glycolate oxidase and hydroxyproline dehydrogenase
Publication date: Available online 2 December 2015 Source:Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease Author(s): Xingsheng Li, John Knight, Sonia Fargue, Brianna Buchalski, Zhengrong Guan, Edward W. Inscho, Abigail Liebow, Kevin Fitzgerald, William Querbes, W. Todd Lowther, Ross P. Holmes Excessive endogenous oxalate synthesis can result in calcium oxalate kidney stone formation and renal failure. Hydroxyproline catabolism in the liver and kidney contributes to endogenous oxalate production in mammals. To quantify this contribution we have infused Wt mice, Agxt KO mice deficient in liver a...
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - December 4, 2015 Category: Molecular Biology Source Type: research

Extracellular matrix-induced Hic-5 expression in glomerular mesangial cells leads to a prosclerotic phenotype independent of TGF-{beta} Research Communication
Chronic fibroproliferative diseases account for approximately 45% of all deaths in the developed world. In the kidney, glomerulosclerosis is the underlying pathology in approximately half of patients with renal failure receiving dialysis. Mesangial cell expression of the LIM protein hydrogen peroxide-induced clone-5 (Hic-5) is important in its pathogenesis. Hic-5 expression increases following mesangial cell attachment to collagen I, associated with increased collagen I expression and increased susceptibility to apoptosis both in vitro and in experimental glomerulosclerosis. TGF-β has an established role in many fibro...
Source: FASEB Journal - December 1, 2015 Category: Biology Authors: Hornigold, N., Mooney, A. Tags: Research Communication Source Type: research

Sialic Acid Rescues Repurified Lipopolysaccharide-Induced Acute Renal Failure via Inhibiting TLR4/PKC/gp91-Mediated Endoplasmic Reticulum Stress, Apoptosis, Autophagy, and Pyroptosis Signaling
In conclusion, early treatment (within 30 min) of SA attenuates rLPS-induced renal failure via the reduction in LPS toxicity and subsequently inhibiting rLPS-activated TLR4/PKC/gp91/ER stress/apoptosis/autophagy/pyroptosis signaling.
Source: Toxicological Sciences - September 17, 2014 Category: Toxicology Authors: Yang, C.-C., Yao, C.-A., Yang, J.-C., Chien, C.-T. Tags: Immunotoxicology Source Type: research

High glucose increases glomerular filtration barrier permeability by activating protein kinase G type Iα subunits in a Nox4-dependent manner.
Abstract Hyperglycemia is a primary factor that disturbs podocyte function in the glomerular filtration process; this disturbance leads to the development of diabetic nephropathy, and ultimately, renal failure. Podocyte function may also be altered by biological agents that modify protein kinase activity, including the cGMP-activated protein kinase type Iα (PKGIα). We hypothesized that hyperglycemia-induced podocyte protein hyperpermeability was dependent on PKGIα activation, and that PKGIα was activated via dimerization induced by reactive oxygen species. This hypothesis was investigated in rat podocytes cult...
Source: Experimental Cell Research - September 13, 2013 Category: Cytology Authors: Piwkowska A, Rogacka D, Audzeyenka I, Angielski S, Jankowski M Tags: Exp Cell Res Source Type: research