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

No abstract is available for this paper.

• Publication year

  2009

• Venue

  Annals medicus

• Publication date

  2009-01-01

• Fields of study

  Medicine

• Identifiers
  DOI 10.1080/07853890902806576PMID 19322705PMCID PMC2932796
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Neuronal RAGE expression modulates severity of injury following transient focal cerebral ischemia.

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• Receptor for advanced glycation end products (RAGE) mediates neuronal differentiation and neurite outgrowth

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• Pathobiological role of advanced glycation endproducts via mitogen-activated protein kinase dependent pathway in the diabetic vasculopathy

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• RAGE, carboxylated glycans and S100A8/A9 play essential roles in colitis-associated carcinogenesis

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• S100A8 and S100A9 Mediate Endotoxin-Induced Cardiomyocyte Dysfunction via the Receptor for Advanced Glycation End Products

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• RAGE modulates myocardial injury consequent to LAD infarction via impact on JNK and STAT signaling in a murine model.

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• AGE/RAGE produces endothelial dysfunction in coronary arterioles in type 2 diabetic mice.

  2008influential reference
• Maturing Dendritic Cells Depend on RAGE for In Vivo Homing to Lymph Nodes1

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• Receptor for Advanced Glycation End Product-Dependent Activation of p38 Mitogen-Activated Protein Kinase Contributes to Amyloid-β-Mediated Cortical Synaptic Dysfunction

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• Receptor for advanced glycation end-products (RAGE) modulates neutrophil adhesion and migration on glycoxidated extracellular matrix.

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• Receptor for Advanced Glycation End Products (RAGE) Deficiency Attenuates the Development of Atherosclerosis in Diabetes

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• High-Mobility Group Box-1 in Ischemia-Reperfusion Injury of the Heart

  2008cited by this paper
• High-mobility group box 1 restores cardiac function after myocardial infarction in transgenic mice.

  2008cited by this paper
• Oxygen Deprivation Triggers Upregulation of Early Growth Response-1 by the Receptor for Advanced Glycation End Products

  2008influential reference
• Receptor for Advanced Glycation End Products (RAGEs) and Experimental Diabetic Neuropathy

  2008cited by this paper
• Vascular and inflammatory stresses mediate atherosclerosis via RAGE and its ligands in apoE-/- mice.

  2008influential reference
• RAGE and Modulation of Ischemic Injury in the Diabetic Myocardium

  2008influential reference
• High-mobility group box protein 1 (HMGB1): an alarmin mediating the pathogenesis of rheumatic disease

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• Inhibition of the RAGE products increases survival in experimental models of severe sepsis and systemic infection

  2007influential reference
• Phosphorylation of Pleckstrin Increases Proinflammatory Cytokine Secretion by Mononuclear Phagocytes in Diabetes Mellitus1

  2007cited by this paper
• The secretion of HMGB1 is required for the migration of maturing dendritic cells

  2007cited by this paper
• Blockade of RAGE Suppresses Alloimmune Reactions In Vitro and Delays Allograft Rejection in Murine Heart Transplantation

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• Neutrophil-derived S100A12 in acute lung injury and respiratory distress syndrome

  2007cited by this paper
• High mobility group box‐1 protein induces the migration and activation of human dendritic cells and acts as an alarmin

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• Toll-like receptor 9–dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE

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• A novel pathway of HMGB1‐mediated inflammatory cell recruitment that requires Mac‐1‐integrin

  2007cited by this paper
• Essential roles of high-mobility group box 1 in the development of murine colitis and colitis-associated cancer.

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• Receptor for Advanced Glycation Endproducts Mediates Neutrophil Migration across Intestinal Epithelium1

  2007influential reference
• Receptor for Advanced Glycation End Products Expression on T Cells Contributes to Antigen-Specific Cellular Expansion In Vivo1

  2007influential reference
• S100B binding to RAGE in microglia stimulates COX‐2 expression

  2007cited by this paper
• Advanced glycation end products induce actin rearrangement and subsequent hyperpermeability of endothelial cells 
THIS ARTICLE HAS BEEN RETRACTED

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• Gene expression changes by amyloid β peptide‐stimulated human postmortem brain microglia identify activation of multiple inflammatory processes

  2006cited by this paper
• Receptor for Advanced-Glycation End Products: Key Modulator of Myocardial Ischemic Injury

  2006cited by this paper
• RAGE modulates vascular inflammation and atherosclerosis in a murine model of type 2 diabetes.

  2006cited by this paper
• Posttranslationally modified proteins as mediators of sustained intestinal inflammation.

  2006cited by this paper
• Suppression of nNOS expression in rat enteric neurones by the receptor for advanced glycation end‐products

  2006cited by this paper
• Key Role of Src Kinase in S100B-induced Activation of the Receptor for Advanced Glycation End Products in Vascular Smooth Muscle Cells*

  2006cited by this paper
• High mobility group box 1 protein interacts with multiple Toll-like receptors.

  2006cited by this paper
• RAGE limits regeneration after massive liver injury by coordinated suppression of TNF-α and NF-κB

  2005influential reference
• Release of High Mobility Group Box 1 by Dendritic Cells Controls T Cell Activation via the Receptor for Advanced Glycation End Products1

  2005cited by this paper
• Advanced glycation end products induce death of retinal neurons via activation of nitric oxide synthase.

  2005cited by this paper
• Requirement of HMGB1 and RAGE for the maturation of human plasmacytoid dendritic cells

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• Exogenous High-Mobility Group Box 1 Protein Induces Myocardial Regeneration After Infarction via Enhanced Cardiac C-Kit+ Cell Proliferation and Differentiation

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• High-mobility group box 1 protein is an inflammatory mediator in necrotizing enterocolitis: protective effect of the macrophage deactivator semapimod.

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• Regulation of monocyte migration by amphoterin (HMGB1).

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• RAGE potentiates Aβ‐induced perturbation of neuronal function in transgenic mice

  2004cited by this paper
• S100B potently activates p65/c-Rel transcriptional complexes in hippocampal neurons: Clinical implications for the role of S100B in excitotoxic brain injury.

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• RAGE modulates peripheral nerve regeneration via recruitment of both inflammatory and axonal outgrowth pathways

  2004cited by this paper
• Blockade of Late Stages of Autoimmune Diabetes by Inhibition of the Receptor for Advanced Glycation End Products1

  2004influential reference
• Blockade of receptor for advanced glycation end product (RAGE) attenuates ischemia and reperfusion injury to the liver in mice

  2004cited by this paper
• S100 protein translocation in response to extracellular S100 is mediated by receptor for advanced glycation endproducts in human endothelial cells.

  2004cited by this paper
• Receptor for advanced glycation end products (RAGE) regulates sepsis but not the adaptive immune response.

  2004cited by this paper
• Monitoring neutrophil activation in juvenile rheumatoid arthritis by S100A12 serum concentrations.

  2004cited by this paper
• Loss of pain perception in diabetes is dependent on a receptor of the immunoglobulin superfamily.

  2004cited by this paper
• Expression of the pro-inflammatory protein S100A12 (EN-RAGE) in rheumatoid and psoriatic arthritis.

  2003cited by this paper
• Central role of RAGE-dependent neointimal expansion in arterial restenosis.

  2003cited by this paper
• The Pattern Recognition Receptor (RAGE) Is a Counterreceptor for Leukocyte Integrins

  2003influential reference
• Neutrophil derived human S100A12 (EN-RAGE) is strongly expressed during chronic active inflammatory bowel disease

  2003cited by this paper
• Suppression of experimental autoimmune encephalomyelitis by selective blockade of encephalitogenic T-cell infiltration of the central nervous system

  2003influential reference
• Expression and function of receptors for advanced glycation end products in bovine corneal endothelial cells.

  2003cited by this paper
• Expression of S100A12 (EN-RAGE) in cystic fibrosis

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• Inflammation-promoting activity of HMGB1 on human microvascular endothelial cells.

  2003cited by this paper
• S100B-RAGE-mediated augmentation of angiotensin II-induced activation of JAK2 in vascular smooth muscle cells is dependent on PLD2.

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• RAGE and arthritis: the G82S polymorphism amplifies the inflammatory response

  2002influential reference
• Release of chromatin protein HMGB1 by necrotic cells triggers inflammation

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• RAGE‐mediated neutrophil dysfunction is evoked by advanced glycation end products (AGEs)

  2002cited by this paper
• RAGE Blockade Stabilizes Established Atherosclerosis in Diabetic Apolipoprotein E–Null Mice

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• Receptor for Advanced Glycation End Products (RAGE) Signaling Induces CREB-dependent Chromogranin Expression during Neuronal Differentiation*

  2002cited by this paper
• N‐Glycans on the receptor for advanced glycation end products influence amphoterin binding and neurite outgrowth

  2002cited by this paper
• Blockade of receptor for advanced glycation end-products restores effective wound healing in diabetic mice.

  2001cited by this paper
• Involvement of microglial receptor for advanced glycation endproducts (RAGE) in Alzheimer's disease: identification of a cellular activation mechanism.

  2001cited by this paper
• Receptor for Advanced Glycation End Products Mediates Inflammation and Enhanced Expression of Tissue Factor in Vasculature of Diabetic Apolipoprotein E–Null Mice

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• Activation of NADPH oxidase by AGE links oxidant stress to altered gene expression via RAGE.

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• Familial Amyloid Polyneuropathy: Receptor for Advanced Glycation End Products-Dependent Triggering of Neuronal Inflammatory and Apoptotic Pathways

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• beta(2)-Microglobulin modified with advanced glycation end products delays monocyte apoptosis.

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• Coregulation of Neurite Outgrowth and Cell Survival by Amphoterin and S100 Proteins through Receptor for Advanced Glycation End Products (RAGE) Activation*

  2000cited by this paper
• Interaction of the Receptor for Advanced Glycation End Products (RAGE) with Transthyretin Triggers Nuclear Transcription Factor kB (NF-kB) Activation

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• N ε-(Carboxymethyl)Lysine Adducts of Proteins Are Ligands for Receptor for Advanced Glycation End Products That Activate Cell Signaling Pathways and Modulate Gene Expression*

  1999cited by this paper
• Receptor for Advanced Glycation End Products (RAGE)-mediated Neurite Outgrowth and Activation of NF-κB Require the Cytoplasmic Domain of the Receptor but Different Downstream Signaling Pathways*

  1999cited by this paper
• RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides.

  1999influential reference
• Advanced glycosylation end products induced tissue factor expression in human monocyte-like U937 cells and increased tissue factor expression in monocytes from diabetic patients.

  1998cited by this paper
• Human blood-brain barrier receptors for Alzheimer's amyloid-beta 1- 40. Asymmetrical binding, endocytosis, and transcytosis at the apical side of brain microvascular endothelial cell monolayer.

  1998cited by this paper
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  1998cited by this paper
• Advanced glycation endproducts inhibit prostacyclin production and induce plasminogen activator inhibitor-1 in human microvascular endothelial cells

  1998cited by this paper
• Inhibition of NF-kappa B activity induces apoptosis in murine hepatocytes.

  1997cited by this paper
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• Activation of the Receptor for Advanced Glycation End Products Triggers a p21 ras -dependent Mitogen-activated Protein Kinase Pathway Regulated by Oxidant Stress*

  1997cited by this paper
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  1996cited by this paper
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  1996cited by this paper
• RAGE and amyloid-beta peptide neurotoxicity in Alzheimer's disease.

  1996influential reference
• The Receptor for Advanced Glycation End Products (RAGE) Is a Cellular Binding Site for Amphoterin

  1995influential reference
• Advanced glycation endproducts interacting with their endothelial receptor induce expression of vascular cell adhesion molecule-1 (VCAM-1) in cultured human endothelial cells and in mice. A potential mechanism for the accelerated vasculopathy of diabetes.

  1995cited by this paper
• Advanced glycation end products (AGEs) on the surface of diabetic erythrocytes bind to the vessel wall via a specific receptor inducing oxidant stress in the vasculature: a link between surface-associated AGEs and diabetic complications.

  1994cited by this paper
• Enhanced cellular oxidant stress by the interaction of advanced glycation end products with their receptors/binding proteins.

  1994cited by this paper
• Receptor for advanced glycation end products (AGEs) has a central role in vessel wall interactions and gene activation in response to circulating AGE proteins.

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• Regulation of human mononuclear phagocyte migration by cell surface-binding proteins for advanced glycation end products.

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• Isolation and characterization of two binding proteins for advanced glycosylation end products from bovine lung which are present on the endothelial cell surface.

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• Abbreviated title: BNIP3 expression in NEC

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