Endothelial dysfunction in patients with chronic kidney disease results from advanced glycation end products (AGE)-mediated inhibition of endothelial nitric oxide synthase through RAGE activation.
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Mechanisms of endothelial dysfunction in resistance arteries from patients with end-stage renal diseaseDangers within: DAMP responses to damage and cell death in kidney disease.A prospective study of frailty in nephrology-referred patients with CKD.Haemodialysis acutely reduces the plasma levels of ADMA without reversing impaired NO-dependent vasodilation.AGER1 regulates endothelial cell NADPH oxidase-dependent oxidant stress via PKC-delta: implications for vascular disease.Skin autofluorescence and all-cause mortality in stage 3 CKD.Hemodialysis removes uremic toxins that alter the biological actions of endothelial cellsDiabetes-related microvascular and macrovascular diseases in the physical therapy settingPeripheral vascular dysfunction in chronic kidney diseaseAssociation of plasma levels of soluble receptor for advanced glycation end products and risk of kidney disease: the Atherosclerosis Risk in Communities studyEvaluation of the EndoPAT as a Tool to Assess Endothelial FunctionEndothelial-cardiomyocyte crosstalk enhances pharmacological cardioprotection.Skin autofluorescence and the association with renal and cardiovascular risk factors in chronic kidney disease stage 3.Risk of Peripheral Artery Occlusive Disease in Patients with Vertigo, Tinnitus, or Sudden Deafness: A Secondary Case-Control Analysis of a Nationwide, Population-Based Health Claims DatabaseInsulin treatment restores islet microvascular vasomotion function in diabetic mice.Uremic Toxicity of Advanced Glycation End Products in CKD.Challenges and opportunities for stem cell therapy in patients with chronic kidney diseaseAdvanced glycation end products and their circulating receptors and level of kidney function in older community-dwelling womenIdentifying advanced glycation end products as a major source of oxidants in aging: implications for the management and/or prevention of reduced renal function in elderly personsIncreased circulating advanced glycation endproducts (AGEs) in acute trauma patients.Ginseng extracts restore high-glucose induced vascular dysfunctions by altering triglyceride metabolism and downregulation of atherosclerosis-related genes.Advanced glycation end product receptor-1 transgenic mice are resistant to inflammation, oxidative stress, and post-injury intimal hyperplasia.Protection against loss of innate defenses in adulthood by low advanced glycation end products (AGE) intake: role of the antiinflammatory AGE receptor-1.Sevelamer revisited: pleiotropic effects on endothelial and cardiovascular risk factors in chronic kidney disease and end-stage renal disease.Diabetes-Induced Reactive Oxygen Species: Mechanism of Their Generation and Role in Renal InjuryPotential for chlorine gas-induced injury in the extrapulmonary vasculature.Naturally occurring inhibitors against the formation of advanced glycation end-products.Similarities and interactions between the ageing process and high chronic intake of added sugars.Role of endoplasmic reticulum stress signalling in diabetic endothelial dysfunction and atherosclerosis.Effect of PKC-β Signaling Pathway on Expression of MCP-1 and VCAM-1 in Different Cell Models in Response to Advanced Glycation End Products (AGEs).The impact of chronic kidney disease and short-term treatment with rosiglitazone on plasma cell-free DNA levels.Skin autofluorescence: a pronounced marker of mortality in hemodialysis patients.Alteration of circulatory platelet microparticles and endothelial microparticles in patients with chronic kidney disease.Pharmacokinetics, pharmacodynamics, and safety of ticagrelor in volunteers with severe renal impairment.Pre-clinical model of severe glutathione peroxidase-3 deficiency and chronic kidney disease results in coronary artery thrombosis and depressed left ventricular function.Uremic Advanced Glycation End Products and Protein-Bound Solutes Induce Endothelial Dysfunction Through Suppression of Krüppel-Like Factor 2.Type 1 diabetic patients have better endothelial function after simultaneous pancreas-kidney transplantation than after kidney transplantation with continued insulin therapy.A new low nephron-CKD model with hypertension, progressive decline of renal function and enhanced inflammation in C57BL/6 mice.AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms.[Correlation between MCP-1, HbA1c and glomerular filtration in nondiabetic patients].
P2860
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P2860
Endothelial dysfunction in patients with chronic kidney disease results from advanced glycation end products (AGE)-mediated inhibition of endothelial nitric oxide synthase through RAGE activation.
description
2008 nî lūn-bûn
@nan
2008 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2008 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
name
Endothelial dysfunction in pat ...... thase through RAGE activation.
@ast
Endothelial dysfunction in pat ...... thase through RAGE activation.
@en
Endothelial dysfunction in pat ...... dvanced glycation end products
@nl
type
label
Endothelial dysfunction in pat ...... thase through RAGE activation.
@ast
Endothelial dysfunction in pat ...... thase through RAGE activation.
@en
Endothelial dysfunction in pat ...... dvanced glycation end products
@nl
prefLabel
Endothelial dysfunction in pat ...... thase through RAGE activation.
@ast
Endothelial dysfunction in pat ...... thase through RAGE activation.
@en
Endothelial dysfunction in pat ...... dvanced glycation end products
@nl
P2093
P2860
P356
P1476
Endothelial dysfunction in pat ...... thase through RAGE activation.
@en
P2093
Ellena Linden
Helen Vlassara
Jaime Uribarri
Jonathan Winston
Weijing Cai
P2860
P304
P356
10.2215/CJN.04291007
P577
2008-02-06T00:00:00Z