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| Ann SchmidtSummaryAffiliation: Columbia University Country: USA Publications
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Publications
RAGE: exacting a toll on the host in response to polymicrobial sepsis and Listeria monocytogenesRaphael Clynes
Department of Medicine and Microbiology, Columbia University Medical Center, 630 West 168th Street, New York, NY 10032, USA
Crit Care 11:183. 2007..In this Commentary, we consider these findings and propose possible mechanisms by which RAGE exacts a heavy toll on the host in response to polymicrobial sepsis and L. monocytogenes...- Soluble RAGE: a hot new biomarker for the hot joint?Bernhard Moser
Department of Surgery, College of Physicians and Surgeons, Columbia University, New York, NY, USA
Arthritis Res Ther 7:142-4. 2005..Nevertheless, although 'cause or effect' relationships may not be established in this report, fascinating insights into RAGE, inflammation and human arthritis emerge from these studies... 
RAGE: a new target for the prevention and treatment of the vascular and inflammatory complications of diabetesA M Schmidt
College of Physicians and Surgeons, 630 West 168th Street, P and S 17 501, Columbia University, New York, NY 10032, USA
Trends Endocrinol Metab 11:368-75. 2000....- Receptor for age (RAGE) is a gene within the major histocompatibility class III region: implications for host response mechanisms in homeostasis and chronic diseaseA M Schmidt
Departments of Surgery, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
Front Biosci 6:D1151-60. 2001..Taken together, an new paradigm is emerging which links RAGE, a gene encoded within the Major Histocompatibility Complex (MHC) Class III regions, to central host response mechanisms in homeostasis and chronic disease... - The role of RAGE in amyloid-beta peptide-mediated pathology in Alzheimer's diseaseAnn Marie Schmidt
Columbia University, College of Physicians and Surgeons, Department of Surgery, 630 West 168th Street, P and S 17 401, New York, NY 10032, USA
Curr Opin Investig Drugs 10:672-80. 2009..These findings suggest that RAGE may mediate a common proinflammatory pathway in neurodegenerative disorders... - Activation of the ROCK1 branch of the transforming growth factor-beta pathway contributes to RAGE-dependent acceleration of atherosclerosis in diabetic ApoE-null miceDe xiu Bu
Division of Surgical Science, Department of Surgery, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY 10032, USA
Circ Res 106:1040-51. 2010..The multiligand RAGE (receptor for advanced glycation end products) contributes to atherosclerosis in apolipoprotein (Apo)E-null mice... - Upregulation of RAGE and its ligands in proliferative retinal diseaseSophia I Pachydaki
Department of Ophthalmology, College of Physician and Surgeons, Columbia University, New York, NY 10032, USA
Exp Eye Res 82:807-15. 2006..These findings suggest a role for the proinflammatory RAGE axis in the pathogenesis of proliferative retinal diseases... - Hypoxia-inducible factor-1 mediates neuronal expression of the receptor for advanced glycation end products following hypoxia/ischemiaPaola Pichiule
Department of Pediatrics, Columbia University, New York, New York 10032, USA
J Biol Chem 282:36330-40. 2007..Specific binding of HIF-1 to this putative HRE in hypoxic cells was detected by chromatin immunoprecipitation assay... - The biology of RAGE and its ligands: uncovering mechanisms at the heart of diabetes and its complicationsShi Fang Yan
Division of Surgical Science, Department of Surgery, Columbia University Medical Center, 630 West 168th Street, P and S 17 501, New York, NY 10032, USA
Curr Diab Rep 7:146-53. 2007..Pharmacologic antagonism of RAGE may hold promise for the treatment of diabetic complications... - RAGE and its ligands: a lasting memory in diabetic complications?Shi Fang Yan
Department of Surgery, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
Diab Vasc Dis Res 1:10-20. 2004..We propose that therapeutic RAGE blockade will intercept maladaptive diabetes-associated memory in the vessel wall and provide cardiovascular protection in diabetes... - RAGE ligand upregulation of VEGF secretion in ARPE-19 cellsWanchao Ma
Departments of Ophthalmology, Columbia University College of Physicians and Surgeons, New York, New York, USA
Invest Ophthalmol Vis Sci 48:1355-61. 2007.... - Protein kinase C beta/early growth response-1 pathway: a key player in ischemia, atherosclerosis, and restenosisShi Fang Yan
Division of Surgical Science, Department of Surgery, Columbia University, New York, New York 10032, USA
J Am Coll Cardiol 48:A47-55. 2006.... - Receptor for advanced glycation end products and the cardiovascular complications of diabetes and beyond: lessons from AGEingShi Fang Yan
Columbia University Medical Center, 630 West 168th Street, P and S 17-501, New York, NY 10032, USA
Endocrinol Metab Clin North Am 35:511-24, viii. 2006..This suggests that blocking the generation or molecular impact of AGEs may modulate the complications of diabetes... - Advanced glycation end products: sparking the development of diabetic vascular injuryAlison Goldin
Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, 75 Francis St, Boston, MA 02115, USA
Circulation 114:597-605. 2006..Because of the emerging evidence about the adverse effects of AGEs on the vasculature of patients with diabetes, a number of different therapies to inhibit AGEs are under investigation... - The ligand/RAGE axis: lighting the fuse and igniting vascular stressShi Fang Yan
Division of Surgical Science, Department of Surgery, Columbia University Medical Center, 630 West 168th Street, P and S 17-501, New York, NY 10032, USA
Curr Atheroscler Rep 8:232-9. 2006..This review focuses on the ligand repertoire of RAGE, the impact of ligand-RAGE interaction, and the potent effect of RAGE blockade in rodent models of vascular injury... - Diabetic vascular disease: it's all the RAGEBarry I Hudson
Department of Surgery, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
Antioxid Redox Signal 7:1588-600. 2005..These observations highlight RAGE as a therapeutic target for treatment of diabetic vascular disease... - Receptor for advanced-glycation end products: key modulator of myocardial ischemic injuryLoredana G Bucciarelli
Division of Surgical Science, Department of Surgery, Columbia University Medical Center, New York, NY 10032, USA
Circulation 113:1226-34. 2006..In this context, our laboratory has been investigating the role of the receptor for advanced-glycation end products (RAGE) in myocardial I/R injury... - RAGE: a journey from the complications of diabetes to disorders of the nervous system - striking a fine balance between injury and repairLing Ling Rong
Department of Surgery, Columbia University Medical Center, NY 10032, USA
Restor Neurol Neurosci 23:355-65. 2005..Experimental evidence supports the premise that RAGE bears both homeostatic and injurious properties in the nervous system, thereby highlighting "yin/yang" features of this receptor and its ligand families... - Infection with a periodontal pathogen increases mononuclear cell adhesion to human aortic endothelial cellsGeorg A Roth
Division of Surgical Science, Department of Surgery, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
Atherosclerosis 190:271-81. 2007.... - Receptor for advanced glycation end products (RAGEs) and experimental diabetic neuropathyCory Toth
University of Calgary, Department of Clinical Neurosciences, Room 155, 3330 Hospital Dr, N W, Calgary, Alberta T2N 4N1, Canada
Diabetes 57:1002-17. 2008..We studied experimental diabetic neuropathy and its relationship with RAGE expression using streptozotocin-induced diabetic mice including a RAGE(-/-) cohort exposed to long-term diabetes compared with littermates without diabetes... - Vascular and inflammatory stresses mediate atherosclerosis via RAGE and its ligands in apoE-/- miceEvis Harja
Division of Surgical Science, Department of Surgery, Columbia University Medical Center, New York, New York 10032, USA
J Clin Invest 118:183-94. 2008..These data highlight unifying mechanisms whereby endothelial RAGE and its ligands mediate vascular and inflammatory stresses that culminate in atherosclerosis in the vulnerable vessel wall... - Receptor for advanced glycation end products expression on T cells contributes to antigen-specific cellular expansion in vivoBernhard Moser
Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA
J Immunol 179:8051-8. 2007..These data indicate that RAGE expressed on T cells is required for efficient priming of T cells and elucidate critical roles for RAGE engagement during cognate dendritic cell-T cell interactions... - RAGE ligation affects T cell activation and controls T cell differentiationYali Chen
Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
J Immunol 181:4272-8. 2008..We conclude that activation of RAGE on T cells is involved in early events that lead to differentiation of Th1(+) T cells... - AGE/RAGE produces endothelial dysfunction in coronary arterioles in type 2 diabetic miceXue Gao
Dept of Internal Medicine, Dalton Cardiovascular Research Center, Univ of Missouri, Columbia, MO 65211, USA
Am J Physiol Heart Circ Physiol 295:H491-8. 2008..These results indicate that AGE/RAGE signaling plays a pivotal role in regulating the production/expression of TNF-alpha, oxidative stress, and endothelial dysfunction in type 2 diabetes... - RAGE and modulation of ischemic injury in the diabetic myocardiumLoredana G Bucciarelli
Division of Surgical Science, Department of Surgery, Columbia University Medical Center, New York, New York, USA
Diabetes 57:1941-51. 2008..In diabetic rat hearts, expression of RAGE and its ligands was enhanced and localized particularly to both endothelial cells and mononuclear phagocytes... 
Receptor for advanced glycation end product-dependent activation of p38 mitogen-activated protein kinase contributes to amyloid-beta-mediated cortical synaptic dysfunctionNicola Origlia
Institute of Neuroscience CNR, Pisa 56100, Italy
J Neurosci 28:3521-30. 2008..Together, our results indicate that Abeta impairs LTP in the entorhinal cortex through neuronal RAGE-mediated activation of p38 MAPK...- Mechanisms of disease: advanced glycation end-products and their receptor in inflammation and diabetes complicationsShi Fang Yan
Division of Surgical Science, Department of Surgery, Columbia University Medical Center, New York, NY 10032, USA
Nat Clin Pract Endocrinol Metab 4:285-93. 2008.... - Receptor for Advanced Glycation Endproducts (RAGE): a formidable force in the pathogenesis of the cardiovascular complications of diabetes & agingShi Fang Yan
Department of Surgery, Columbia University Medical Center, New York, NY 10032, USA
Curr Mol Med 7:699-710. 2007..We conclude that antagonism of RAGE may reflect a novel and therapeutically logical and safe target in cardiovascular stress induced by aging and chronic diabetes... - Oxygen deprivation triggers upregulation of early growth response-1 by the receptor for advanced glycation end productsJong Sun Chang
Division of Surgical Science, Department of Surgery, Columbia University Medical Center, New York, NY 10032, USA
Circ Res 102:905-13. 2008..These findings identify RAGE as a master regulator of tissue stress elicited by hypoxia and highlight this receptor as a central therapeutic target to suppress the tissue injury-provoking effects of oxygen deprivation... - RAGE mediates podocyte injury in adriamycin-induced glomerulosclerosisJiancheng Guo
Department of Surgery, Columbia University Medical Center, New York, New York 10025, USA
J Am Soc Nephrol 19:961-72. 2008..These data suggest that RAGE may contribute to the pathogenesis of podocyte injury in sclerosing glomerulopathies such as focal segmental glomerulosclerosis... - RAGE modulates myocardial injury consequent to LAD infarction via impact on JNK and STAT signaling in a murine modelAlexey Aleshin
Department of Surgery, Columbia University, New York, NY 10032, USA
Am J Physiol Heart Circ Physiol 294:H1823-32. 2008.... - PKCbeta modulates ischemia-reperfusion injury in the heartLinghua Kong
Dept of Surgery, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
Am J Physiol Heart Circ Physiol 294:H1862-70. 2008..These data implicate PKCbeta in I/R-mediated myocardial injury, at least in part via phosphorylation of JNK, and suggest that blockade of PKCbeta may represent a potent strategy to protect the vulnerable myocardium... - The expression of the receptor for glycation endproducts (RAGE) in oral squamous cell carcinomasRegina Landesberg
Division of Oral and Maxillofacial Surgery, College of Dental Medicine, Columbia University, New York, New York 10032, USA
Oral Surg Oral Med Oral Pathol Oral Radiol Endod 105:617-24. 2008..Higher expression was observed in the normal tissues compared to the OSCCs. Our results show that RAGE immunoreactivity correlates with histologic differentiation in OSCC... - Identification, classification, and expression of RAGE gene splice variantsBarry I Hudson
Division of Surgical Science, Department of Surgery, College of Physicians and Surgeons, Columbia University, 630 W 168th St, PS 17 401, New York, New York 10032, USA
FASEB J 22:1572-80. 2008..Taken together, identification of functional splice variants of RAGE underscores the biological diversity of the RAGE gene and will aid in the understanding of the gene in the normal and pathological state... - The RAGE axis and endothelial dysfunction: maladaptive roles in the diabetic vasculature and beyondRavichandran Ramasamy
Division of Surgical Science, Department of Surgery, Columbia University Medical Center, 630 West 168th Street, New York, NY 10032, USA
Trends Cardiovasc Med 15:237-43. 2005..These considerations support the premise that the ligand-RAGE axis may be an important target for therapeutic intervention in cardiovascular disease and, fundamentally, in initiation and amplification of inflammatory responses... - RAGE modulates vascular inflammation and atherosclerosis in a murine model of type 2 diabetesThoralf Wendt
Department of Surgery, College of Physicians and Surgeons of Columbia University, 630 W, 168th Street, Black Building 1705, New York, NY 10032, USA
Atherosclerosis 185:70-7. 2006..Taken together, these findings establish a new murine model for the study of atherosclerosis in type 2 diabetes and highlight important roles for RAGE in proatherogenic mechanisms in hyperglycemia triggered by insulin resistance... - The RAGE axis in early diabetic retinopathyGaetano R Barile
Department of Ophthalmology, Mailman School of Public Health, Columbia University, New York, NY, USA
Invest Ophthalmol Vis Sci 46:2916-24. 2005..This study was conducted to characterize the role of the RAGE axis in a murine model of nonproliferative diabetic retinopathy (NPDR)... - S100P stimulates cell proliferation and survival via receptor for activated glycation end products (RAGE)Thiruvengadam Arumugam
Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan 48109, USA
J Biol Chem 279:5059-65. 2004..These data suggest that S100P can act in an autocrine manner via RAGE to stimulate cell proliferation and survival... - Blockade of receptor for advanced glycation endproducts: a new target for therapeutic intervention in diabetic complications and inflammatory disordersBarry I Hudson
Department of Surgery, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
Arch Biochem Biophys 419:80-8. 2003..Here, we will summarize the known consequences of RAGE activation in the tissues and highlight novel areas for therapeutic intervention in these disease states... - S100B-RAGE-mediated augmentation of angiotensin II-induced activation of JAK2 in vascular smooth muscle cells is dependent on PLD2Sean S Shaw
Vascular Biology Center, Medical College of Georgia, Augusta, Georgia 30912, USA
Diabetes 52:2381-8. 2003..These results provide direct evidence for linkages between PLD2, ROS production, and S100B-RAGE-induced enhancement of Ang II-induced cell proliferation and activation of JAK2 in VSMCs... - The receptor RAGE as a progression factor amplifying arachidonate-dependent inflammatory and proteolytic response in human atherosclerotic plaques: role of glycemic controlFrancesco Cipollone
University of Chieti G D'Annunzio School of Medicine, Chieti, Italy
Circulation 108:1070-7. 2003.... - Oral infection with a periodontal pathogen accelerates early atherosclerosis in apolipoprotein E-null miceEvanthia Lalla
Division of Periodontics, School of Dental and Oral Surgery, Columbia University, New York, NY 10032, USA
Arterioscler Thromb Vasc Biol 23:1405-11. 2003.... - Receptor for AGE (RAGE) mediates neointimal formation in response to arterial injuryZhongmin Zhou
Experimental Interventional Laboratory, Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
Circulation 107:2238-43. 2003..CONCLUSIONS: These findings indicate that RAGE/ligand interaction plays a key role in neointimal formation after vascular injury irrespective of diabetes status and suggest a novel target to minimize neointimal hyperplasia... - Central role of RAGE-dependent neointimal expansion in arterial restenosisTaichi Sakaguchi
Department of Surgery, College of Physicians and Surgeons, Columbia University, New York, New York, USA
J Clin Invest 111:959-72. 2003..Taken together, these data highlight key roles for RAGE in modulating smooth muscle cell properties after injury and suggest that RAGE is a logical target for suppression of untoward neointimal expansion consequent to arterial injury... - RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathyThoralf M Wendt
Department of Pathology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
Am J Pathol 162:1123-37. 2003.... - Suppression of experimental autoimmune encephalomyelitis by selective blockade of encephalitogenic T-cell infiltration of the central nervous systemShirley ShiDu Yan
Department of Pathology, College of Physicians and Surgeons of Columbia University, New York, New York, USA
Nat Med 9:287-93. 2003..These data reinforce the importance of RAGE-ligand interactions in modulating properties of CD4+ T cells that infiltrate the CNS... - Receptor for advanced glycation endproducts: a multiligand receptor magnifying cell stress in diverse pathologic settingsDavid Stern
Department of Surgery, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
Adv Drug Deliv Rev 54:1615-25. 2002..These observations suggest that RAGE might represent a therapeutic target in a diverse group of seemingly unrelated disorders linked only by a multiligand receptor with an unusually wide and diverse repertoire of ligands, namely, RAGE... - RAGE blockade stabilizes established atherosclerosis in diabetic apolipoprotein E-null miceLoredana G Bucciarelli
Division of Surgical Science, College of Physicians and Surgeons, Department of Surgery, Columbia University, New York, NY 10032, USA
Circulation 106:2827-35. 2002..Blockade of RAGE may be a novel strategy to stabilize atherosclerosis and vascular inflammation in established diabetes... - Receptor for advanced glycation endproducts (RAGE) and the complications of diabetesDavid M Stern
Department of Surgery, College of Physicians, Columbia University, P and S 17 401, West 168th Street, New York, NY 10032, USA
Ageing Res Rev 1:1-15. 2002.... - Receptor for advanced glycation end products on human synovial fibroblasts: role in the pathogenesis of dialysis-related amyloidosisFan Fan Hou
Division of Nephrology, Nanfang Hospital, Guangzhou, People s Republic of China
J Am Soc Nephrol 13:1296-306. 2002..These data provide evidence of RAGE-mediated perturbation of human synoviocytes, which may be involved in the pathogenesis of inflammatory processes associated with DRA... - Receptor for advanced glycation endproducts (RAGE) and vascular inflammation: insights into the pathogenesis of macrovascular complications in diabetesThoralf Wendt
Division of Surgical Science, Department of Surgery, Columbia University College of Physicians and Surgeons, 630 West 168th Street, P and S 17-401, New York, NY 10032, USA
Curr Atheroscler Rep 4:228-37. 2002..Insights into therapeutic strategies to prevent or interrupt these processes are presented... - Glycation, inflammation, and RAGE: a scaffold for the macrovascular complications of diabetes and beyondShi Fang Yan
Department of Surgery, College of Physicians and Surgeons, Columbia University, 630 W 168th St, New York, NY 10032, USA
Circ Res 93:1159-69. 2003..We propose that antagonism of RAGE will provide a unique means to dismantle this scaffold and, thereby, suppress initiation/progression of vascular disease and cardiac dysfunction that accompany diabetes and aging... - Early growth response-1 promotes atherogenesis: mice deficient in early growth response-1 and apolipoprotein E display decreased atherosclerosis and vascular inflammationEvis Harja
Department of Surgery, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
Circ Res 94:333-9. 2004..We conclude that Egr-1 broadly regulates expression of molecules critically linked to atherogenesis and lesion progression... - Aldose reductase and AGE-RAGE pathways: key players in myocardial ischemic injuryMichiyo Kaneko
Division of Surgical Science, P and S 17-401, Columbia University Medical Center, 630 West 168th St, New York, NY 10032, USA
Ann N Y Acad Sci 1043:702-9. 2005..The potent impact of increased flux via the aldose reductase pathway and the increased AGE interactions with its receptor (RAGE) resulting in cardiac dysfunction will be discussed in this chapter... - Receptor for advanced glycation end products and its ligands: a journey from the complications of diabetes to its pathogenesisWilliam Kim
Division of Surgical Science, Department of Surgery, Columbia University Medical Center, 630 West 168th St, P and S 17-501, New York, New York 10032, USA
Ann N Y Acad Sci 1043:553-61. 2005..Studies are in progress to test the premise that antagonism of this interaction is a logical strategy for the prevention and treatment of diabetes... - RAGE and amyloid beta interactions: atomic force microscopy and molecular modelingMichael O Chaney
Department of Surgery, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA
Biochim Biophys Acta 1741:199-205. 2005..Our modeling suggests that a soluble dimeric RAGE assembly creates a positively charged well into which the negative charges of the N-terminal domain of dimeric Abeta dock... - Mechanisms for the induction of HNE- MDA- and AGE-adducts, RAGE and VEGF in retinal pigment epithelial cellsJilin Zhou
Department of Ophthalmology, Columbia University, 630 W. 168th St, New York, NY 10032, USA
Exp Eye Res 80:567-80. 2005.... - Advanced glycation end products and RAGE: a common thread in aging, diabetes, neurodegeneration, and inflammationRavichandran Ramasamy
Department of Surgery, Columbia University Medical Center, New York, NY 10032, USA
Glycobiology 15:16R-28R. 2005..Thus, we propose that targeting this pathway may represent a logical step in the prevention/treatment of the sequelae of these disorders... - Chronic vascular inflammation in patients with type 2 diabetes: endothelial biopsy and RT-PCR analysisLei Feng
Department of Radiology, New York Presbyterian Hospital, 177 Fort Washington Ave, MHB 8SK, New York, NY 10032, USA
Diabetes Care 28:379-84. 2005.... - Central role of PKCbeta in neointimal expansion triggered by acute arterial injuryMartin Andrassy
Department of Surgery, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA
Circ Res 96:476-83. 2005..These data highlight novel roles for PKCbeta in the SMC response to acute arterial injury and suggest that blockade of PKCbeta may represent a therapeutic strategy to limit restenosis... - Advanced glycation end products and vascular inflammation: implications for accelerated atherosclerosis in diabetesGiuseppina Basta
CNR Institute of Clinical Physiology, Pisa, Italy
Cardiovasc Res 63:582-92. 2004..Thus, a better understanding of the biochemical mechanisms by which AGEs contribute to such processes in the vessel wall could be relevant to devise preventive and therapeutic strategies for diabetic atherosclerosis... - Protein glycation: a firm link to endothelial cell dysfunctionJean-Luc Wautier
University Lariboisiere-Saint Louis and Institut National de la Transfusion Sanguine, Paris, France
Circ Res 95:233-8. 2004..Thus, agents that limit AGE formation, increase the catabolism of these species, or antagonize their binding to RAGE may provide new targets for vascular protection in diabetes... - RAGE: a novel target for drug intervention in diabetic vascular diseaseBarry I Hudson
College of Physicians and Surgeons, Columbia University, New York, New York, USA
Pharm Res 21:1079-86. 2004..In conclusion, RAGE is a target for drug development to prevent vascular disease in diabetic and nondiabetic subjects... - Central role for aldose reductase pathway in myocardial ischemic injuryYuying C Hwang
Department of Surgery, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
FASEB J 18:1192-9. 2004..We propose that interventions targeting AR may provide a novel adjunctive approach to protect ischemic myocardium... - Enhanced expression of receptor for advanced glycation end products in chronic kidney diseaseFan Fan Hou
Division of Nephrology, Nanfang Hospital, Guangzhou, People s Republic of China
J Am Soc Nephrol 15:1889-96. 2004..It was concluded that RAGE expression was upregulated on monocytes from patients with CKD. Enhanced RAGE may amplify AGE-induced monocytes perturbation and contribute to monocyte-mediated systemic inflammation in progressive CKD... - RAGE axis: Animal models and novel insights into the vascular complications of diabetesYoshifumi Naka
Department of Surgery, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
Arterioscler Thromb Vasc Biol 24:1342-9. 2004..Future studies must rigorously test the potential impact of RAGE blockade in human subjects; such trials are on the horizon... - Blockade of receptor for advanced glycation end product (RAGE) attenuates ischemia and reperfusion injury to the liver in miceShan Zeng
Division of Liver Diseases and Transplantation, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA
Hepatology 39:422-32. 2004..We propose that blockade of this pathway may represent a novel strategy to attenuate injury in hepatic I/R and to facilitate regeneration... - Advanced glycation end products activate endothelium through signal-transduction receptor RAGE: a mechanism for amplification of inflammatory responsesGiuseppina Basta
CNR Institute of Clinical Physiology, Pisa, Italy
Circulation 105:816-22. 2002..CONCLUSIONS: AGEs, through RAGE, may prime proinflammatory mechanisms in endothelial cells, thereby amplifying proinflammatory mechanisms in atherogenesis and chronic inflammatory disorders...
Research Grants
- RAGE and a Novel Tumor AxisAnn Schmidt; Fiscal Year: 2005....