Unlocking the biology of RAGE in diabetic microvascular complications

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Suppression of accelerated diabetic atherosclerosis by the soluble receptor for advanced glycation endproducts

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Projecting the Number of Patients with End-Stage Renal Disease in the United States to the Year 2015

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Increased accumulation of the glycoxidation product N(epsilon)-(carboxymethyl)lysine in human tissues in diabetes and aging.

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RAGE Drives the Development of Glomerulosclerosis and Implicates Podocyte Activation in the Pathogenesis of Diabetic Nephropathy

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The Pattern Recognition Receptor (RAGE) Is a Counterreceptor for Leukocyte Integrins

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Expression of Advanced Glycation End Products and Their Cellular Receptor RAGE in Diabetic Nephropathy and Nondiabetic Renal Disease

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Trends in childhood type 1 diabetes incidence in Europe during 1989–2008: evidence of non-uniformity over time in rates of increase

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Glycation, Glycoxidation, and Cross-Linking of Collagen by Glucose: Kinetics, Mechanisms, and Inhibition of Late Stages of the Maillard Reaction

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Randomized Trial of an Inhibitor of Formation of Advanced Glycation End Products in Diabetic Nephropathy

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Glycation and Carboxymethyllysine Levels in Skin Collagen Predict the Risk of Future 10-Year Progression of Diabetic Retinopathy and Nephropathy in the Diabetes Control and Complications Trial and Epidemiology of Diabetes Interventions and Complications Participants With Type 1 Diabetes

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Microvascular lesions of diabetic retinopathy: clues towards understanding pathogenesis?

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The RAGE axis: A fundamental mechanism signaling danger to the vulnerable vasculature

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Role of the Maillard Reaction in Aging of Tissue Proteins

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Interaction of the RAGE Cytoplasmic Domain with Diaphanous-1 Is Required for Ligand-stimulated Cellular Migration through Activation of Rac1 and Cdc42

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Therapies for hyperglycaemia-induced diabetic complications: from animal models to clinical trials

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Diabetic Painful and Insensate Neuropathy: Pathogenesis and Potential Treatments

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S100P Stimulates Cell Proliferation and Survival via Receptor for Activated Glycation End Products (RAGE)

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Role of Advanced Glycation End Products and Their Receptors in Development of Diabetic Neuropathy

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Receptor for Advanced Glycation End Products Activation Injures Primary Sensory Neurons via Oxidative Stress

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Formation of glyoxal, methylglyoxal and 3-deoxyglucosone in the glycation of proteins by glucose

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Skin Autofluorescence

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Renal catabolism of advanced glycation end products: the fate of pentosidine

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Advanced glycation end products and their receptors co-localise in rat organs susceptible to diabetic microvascular injury

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Methylglyoxal promotes oxidative stress and endothelial dysfunction

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Septic Shock Is Associated with Receptor for Advanced Glycation End Products Ligation of LPS

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Hyperglycaemia-induced pro-inflammatory responses by retinal Müller glia are regulated by the receptor for advanced glycation end-products (RAGE)

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Mechanisms of islet amyloidosis toxicity in type 2 diabetes

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The RAGE Axis in Early Diabetic Retinopathy

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Effect of Aminoguanidine on Functional and Structural Abnormalities in Peripheral Nerve of STZ-Induced Diabetic Rats

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The Prevalence of Diabetic Retinopathy Among Adult Type1 Diabetic Persons in the United States

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Deletion of the Receptor for Advanced Glycation End Products Reduces Glomerulosclerosis and Preserves Renal Function in the Diabetic OVE26 Mouse

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Epithelial-Mesenchymal Transition as a Potential Explanation for Podocyte Depletion in Diabetic Nephropathy

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sRAGE and Risk of Diabetes, Cardiovascular Disease, and Death

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Total Soluble and Endogenous Secretory Receptor for Advanced Glycation End Products as Predictive Biomarkers of Coronary Heart Disease Risk in Patients With Type 2 Diabetes

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Inhibition of Diabetic Leukostasis and Blood-Retinal Barrier Breakdown with a Soluble Form of a Receptor for Advanced Glycation End Products

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Tempering the wrath of RAGE: An emerging therapeutic strategy against diabetic complications, neurodegeneration, and inflammation

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Homodimerization Is Essential for the Receptor for Advanced Glycation End Products (RAGE)-mediated Signal Transduction

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Induction of high mobility group box-1 in dorsal root ganglion contributes to pain hypersensitivity after peripheral nerve injury

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Signal Transduction in Receptor for Advanced Glycation End Products (RAGE)

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Advanced Glycation End Product (AGE)-Receptor for AGE (RAGE) Signaling and Up-regulation of Egr-1 in Hypoxic Macrophages

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Lysophosphatidic acid targets vascular and oncogenic pathways via RAGE signaling

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Increasing Incidence of Type 1 Diabetes in Youth

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Metformin Inhibits Advanced Glycation End Products (AGEs)-induced Renal Tubular Cell Injury by Suppressing Reactive Oxygen Species Generation via Reducing Receptor for AGEs (RAGE) Expression

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Circulating soluble RAGE as a predictive biomarker of cardiovascular event risk in patients with type 2 diabetes

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Metabolic memory: Mechanisms and implications for diabetic retinopathy

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Pentosidine as a biomarker for microvascular complications in type 2 diabetic patients

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RAGE Deficiency Improves Postinjury Sciatic Nerve Regeneration in Type 1 Diabetic Mice

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Pancreatic cancer-derived S-100A8 N-terminal peptide: A diabetes cause?

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Stable RAGE-Heparan Sulfate Complexes Are Essential for Signal Transduction

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High-mobility group box-1 protein activates inflammatory signaling pathway components and disrupts retinal vascular-barrier in the diabetic retina

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Pravastatin inhibits advanced glycation end products (AGEs)-induced proximal tubular cell apoptosis and injury by reducing receptor for AGEs (RAGE) level

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Ten-Year Change in Vision-Related Quality of Life in Type 1 Diabetes: Wisconsin Epidemiologic Study of Diabetic Retinopathy

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DNA Aptamer Raised Against AGEs Blocks the Progression of Experimental Diabetic Nephropathy

Kaida, Y., Fukami, K., Matsui, T., Higashimoto, Y., Nishino, Y., Obara, N., Nakayama, Y., Ando, R., Toyonaga, M., Ueda, S., et al. (2013) · Diabetes · doi:10.2337/db12-1608 · Cited by 78 · see citing works

The Role of High-Mobility Group Box-1 Protein in the Development of Diabetic Nephropathy

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RAGE binds C1q and enhances C1q-mediated phagocytosis

Ma, W., Rai, V., Hudson, B. I., Song, F., Schmidt, A. M., & Barile, G. R. (2012) · Cellular Immunology · doi:10.1016/j.cellimm.2012.02.001 · Cited by 73 · see citing works

Advanced glycation endproducts in peripheral nerve in type 2 diabetes with neuropathy

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Aldose Reductase and AGE–RAGE pathways: central roles in the pathogenesis of vascular dysfunction in aging rats

Hallam, K. M., Li, Q., Ananthakrishnan, R., Kalea, A. Z., Zou, Y. S., Vedantham, S., Schmidt, A. M., Yan, S. F., & Ramasamy, R. (2010) · Aging Cell · doi:10.1111/j.1474-9726.2010.00606.x · Cited by 57 · see citing works

The association between skin collagen glucosepane and past progression of microvascular and neuropathic complications in type 1 diabetes

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Serum Levels of Advanced Glycation Endproducts and Other Markers of Protein Damage in Early Diabetic Nephropathy in Type 1 Diabetes

Perkins, B. A., Rabbani, N., Weston, A. J., Ficociello, L., Adaikalakoteswari, A., Niewczas, M. A., Warram, J. H., Królewski, A. S., & Thornalley, P. J. (2012) · PLoS ONE · doi:10.1371/journal.pone.0035655 · Cited by 54 · see citing works

What you can't feel can hurt you

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Levels of Soluble Advanced Glycation End Product-Receptors and Other Soluble Serum Markers as Indicators of Diabetic Neuropathy in the Foot

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Elevated serum levels of AGEs, sRAGE, and pentosidine in Tunisian patients with severity of diabetic retinopathy

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Plasma advanced glycation endproduct, methylglyoxal-derived hydroimidazolone is elevated in young, complication-free patients with Type 1 diabetes

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Neurogenic factor-induced Langerhans cell activation in diabetic mice with mechanical allodynia

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Expression of lysophosphatidic acid, autotaxin and acylglycerol kinase as biomarkers in diabetic retinopathy

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Lysophospholipid interactions with protein targets

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Prevention of arterial stiffening by pyridoxamine in diabetes is associated with inhibition of the pathogenic glycation on aortic collagen

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Puerarin enhances superoxide dismutase activity and inhibits RAGE and VEGF expression in retinas of STZ–induced early diabetic rats

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