Glucose, glycation, and RAGE: implications for amplification of cellular dysfunction in diabetic nephropathy. - Wikidata - awgldk - TriplyDB

Glucose, glycation, and RAGE: implications for amplification of cellular dysfunction in diabetic nephropathy.

Glucose, glycation, and RAGE: implications for amplification of cellular dysfunction in diabetic nephropathy.

http://www.wikidata.org/entity/Q35111728

about

Low levels of serum soluble receptors for advanced glycation end products, biomarkers for disease state: myth or reality Site-specific AGE modifications in the extracellular matrix: a role for glyoxal in protein damage in diabetes Identification of mouse orthologue of endogenous secretory receptor for advanced glycation end-products: structure, function and expression The expression of RAGE and EN-RAGE in leprosy.Cardiac fibroblast-dependent extracellular matrix accumulation is associated with diastolic stiffness in type 2 diabetes N-glycosylation of carnosinase influences protein secretion and enzyme activity: implications for hyperglycemia Pretreatment with the total flavone glycosides of Flos Abelmoschus manihot and hyperoside prevents glomerular podocyte apoptosis in streptozotocin-induced diabetic nephropathy.Amylin deposition in the brain: A second amyloid in Alzheimer disease?A glimpse of matrix metalloproteinases in diabetic nephropathy.Advanced glycation end product (AGE) receptor 1 suppresses cell oxidant stress and activation signaling via EGF receptor Manifestation of renal disease in obesity: pathophysiology of obesity-related dysfunction of the kidney Alternative splicing of the RAGE cytoplasmic domain regulates cell signaling and function.Genomic damage in endstage renal disease-contribution of uremic toxins 17beta-Estradiol attenuates diabetic kidney disease by regulating extracellular matrix and transforming growth factor-beta protein expression and signaling A clinical comparative study of the management of chronic renal failure with Punarnavadi compound.Posttranslationally modified proteins as mediators of sustained intestinal inflammation.Anti-atherosclerotic effects of sitagliptin in patients with type 2 diabetes mellitus.Icariside II ameliorates diabetic nephropathy in streptozotocin-induced diabetic rats Targeting AGEs Signaling Ameliorates Central Nervous System Diabetic Complications in Rats Significance of proximal tubular metabolism of advanced glycation end products in kidney diseases.The podocyte: from bench to bedside.Role of the JAK/STAT signaling pathway in diabetic nephropathy.Premature senescence of endothelial cells: Methusaleh's dilemma.AGEs and glucose levels modulate type I and III procollagen mRNA synthesis in dermal fibroblasts cells culture Alagebrium inhibits neointimal hyperplasia and restores distributions of wall shear stress by reducing downstream vascular resistance in obese and diabetic rats.Diabetes and hypertension: epidemiology of the relationship and pathophysiology of factors associated with these comorbid conditions.Crystal structure of the deglycating enzyme fructosamine oxidase (amadoriase II)Receptor for advanced glycation end products: its role in Alzheimer's disease and other neurological diseases.Heat-processed Panax ginseng and diabetic renal damage: active components and action mechanism.Poly(Adenosine 5'-diphosphate-ribose) polymerase inhibition counteracts multiple manifestations of experimental type 1 diabetic nephropathy.SIRT4 overexpression protects against diabetic nephropathy by inhibiting podocyte apoptosis.Diabetic microvascular complications: possible targets for improved macrovascular outcomes A novel improved therapy strategy for diabetic nephropathy: targeting AGEs.The renal endothelium in diabetic nephropathy.Molecular mechanisms of AGE/RAGE-mediated fibrosis in the diabetic heart.Ezrin contributes to impaired podocyte migration and adhesion caused by advanced glycation end products.Do Advanced Glycation End Products and Its Receptor Play a Role in Pathophysiology of Hypertension?Impaired transcription factor interplay in addition to advanced glycation end products suppress podocalyxin expression in high glucose-treated human podocytes.Acute effect of high glucose on long-term cell growth: a role for transient glucose increase in proximal tubule cell injury.Is Elevated Levels of Serum Soluble Receptor for Advanced Glycation End Products Harmful in Cigarette Smokers?

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Glucose, glycation, and RAGE: implications for amplification of cellular dysfunction in diabetic nephropathy.

http://www.wikidata.org/entity/Q35111728

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2003 nî lūn-bûn

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Ann Marie Schmidt

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Bernd Arnold

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Jiancheng Guo

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Nozomu Tanji

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Peter P Nawroth

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Ravichandran Ramasamy

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Shi Fang Yan

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advanced glycation end-product receptor activity