Ann Schmidt

Summary

Affiliation: Columbia University
Country: USA

Publications

  1. ncbi The role of RAGE in amyloid-beta peptide-mediated pathology in Alzheimer's disease
    Ann 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
  2. pmc RAGE: exacting a toll on the host in response to polymicrobial sepsis and Listeria monocytogenes
    Raphael Clynes
    Department of Medicine and Microbiology, Columbia University Medical Center, 630 West 168th Street, New York, NY 10032, USA
    Crit Care 11:183. 2007
  3. pmc 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
  4. ncbi RAGE: a new target for the prevention and treatment of the vascular and inflammatory complications of diabetes
    A 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
  5. ncbi Receptor for age (RAGE) is a gene within the major histocompatibility class III region: implications for host response mechanisms in homeostasis and chronic disease
    A M Schmidt
    Departments of Surgery, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA
    Front Biosci 6:D1151-60. 2001
  6. pmc Activation of the ROCK1 branch of the transforming growth factor-beta pathway contributes to RAGE-dependent acceleration of atherosclerosis in diabetic ApoE-null mice
    De 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
  7. ncbi Upregulation of RAGE and its ligands in proliferative retinal disease
    Sophia I Pachydaki
    Department of Ophthalmology, College of Physician and Surgeons, Columbia University, New York, NY 10032, USA
    Exp Eye Res 82:807-15. 2006
  8. ncbi Hypoxia-inducible factor-1 mediates neuronal expression of the receptor for advanced glycation end products following hypoxia/ischemia
    Paola Pichiule
    Department of Pediatrics, Columbia University, New York, New York 10032, USA
    J Biol Chem 282:36330-40. 2007
  9. ncbi The biology of RAGE and its ligands: uncovering mechanisms at the heart of diabetes and its complications
    Shi 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
  10. ncbi 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

Research Grants

  1. RAGE and a Novel Tumor Axis
    Ann Schmidt; Fiscal Year: 2005

Collaborators

Detail Information

Publications68

  1. ncbi The role of RAGE in amyloid-beta peptide-mediated pathology in Alzheimer's disease
    Ann 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...
  2. pmc RAGE: exacting a toll on the host in response to polymicrobial sepsis and Listeria monocytogenes
    Raphael 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...
  3. pmc 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...
  4. ncbi RAGE: a new target for the prevention and treatment of the vascular and inflammatory complications of diabetes
    A 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
    ....
  5. ncbi Receptor for age (RAGE) is a gene within the major histocompatibility class III region: implications for host response mechanisms in homeostasis and chronic disease
    A 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...
  6. pmc Activation of the ROCK1 branch of the transforming growth factor-beta pathway contributes to RAGE-dependent acceleration of atherosclerosis in diabetic ApoE-null mice
    De 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...
  7. ncbi Upregulation of RAGE and its ligands in proliferative retinal disease
    Sophia 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...
  8. ncbi Hypoxia-inducible factor-1 mediates neuronal expression of the receptor for advanced glycation end products following hypoxia/ischemia
    Paola 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...
  9. ncbi The biology of RAGE and its ligands: uncovering mechanisms at the heart of diabetes and its complications
    Shi 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...
  10. ncbi 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...
  11. ncbi RAGE ligand upregulation of VEGF secretion in ARPE-19 cells
    Wanchao Ma
    Departments of Ophthalmology, Columbia University College of Physicians and Surgeons, New York, New York, USA
    Invest Ophthalmol Vis Sci 48:1355-61. 2007
    ....
  12. ncbi Protein kinase C beta/early growth response-1 pathway: a key player in ischemia, atherosclerosis, and restenosis
    Shi 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
    ....
  13. ncbi Receptor for advanced glycation end products and the cardiovascular complications of diabetes and beyond: lessons from AGEing
    Shi 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...
  14. ncbi Advanced glycation end products: sparking the development of diabetic vascular injury
    Alison 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...
  15. ncbi The ligand/RAGE axis: lighting the fuse and igniting vascular stress
    Shi 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...
  16. ncbi Diabetic vascular disease: it's all the RAGE
    Barry 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...
  17. ncbi Receptor for advanced-glycation end products: key modulator of myocardial ischemic injury
    Loredana 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...
  18. ncbi RAGE: a journey from the complications of diabetes to disorders of the nervous system - striking a fine balance between injury and repair
    Ling 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...
  19. ncbi Infection with a periodontal pathogen increases mononuclear cell adhesion to human aortic endothelial cells
    Georg 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
    ....
  20. ncbi Receptor for advanced glycation end products (RAGEs) and experimental diabetic neuropathy
    Cory 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...
  21. pmc Vascular and inflammatory stresses mediate atherosclerosis via RAGE and its ligands in apoE-/- mice
    Evis 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...
  22. ncbi Receptor for advanced glycation end products expression on T cells contributes to antigen-specific cellular expansion in vivo
    Bernhard 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...
  23. pmc RAGE ligation affects T cell activation and controls T cell differentiation
    Yali 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...
  24. pmc AGE/RAGE produces endothelial dysfunction in coronary arterioles in type 2 diabetic mice
    Xue 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...
  25. pmc RAGE and modulation of ischemic injury in the diabetic myocardium
    Loredana 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...
  26. doi Receptor for advanced glycation end product-dependent activation of p38 mitogen-activated protein kinase contributes to amyloid-beta-mediated cortical synaptic dysfunction
    Nicola 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...
  27. doi Mechanisms of disease: advanced glycation end-products and their receptor in inflammation and diabetes complications
    Shi 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
    ....
  28. ncbi Receptor for Advanced Glycation Endproducts (RAGE): a formidable force in the pathogenesis of the cardiovascular complications of diabetes & aging
    Shi 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...
  29. doi Oxygen deprivation triggers upregulation of early growth response-1 by the receptor for advanced glycation end products
    Jong 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...
  30. pmc RAGE mediates podocyte injury in adriamycin-induced glomerulosclerosis
    Jiancheng 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...
  31. doi RAGE modulates myocardial injury consequent to LAD infarction via impact on JNK and STAT signaling in a murine model
    Alexey Aleshin
    Department of Surgery, Columbia University, New York, NY 10032, USA
    Am J Physiol Heart Circ Physiol 294:H1823-32. 2008
    ....
  32. doi PKCbeta modulates ischemia-reperfusion injury in the heart
    Linghua 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...
  33. doi The expression of the receptor for glycation endproducts (RAGE) in oral squamous cell carcinomas
    Regina 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...
  34. ncbi Identification, classification, and expression of RAGE gene splice variants
    Barry 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...
  35. ncbi The RAGE axis and endothelial dysfunction: maladaptive roles in the diabetic vasculature and beyond
    Ravichandran 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...
  36. ncbi RAGE modulates vascular inflammation and atherosclerosis in a murine model of type 2 diabetes
    Thoralf 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...
  37. ncbi The RAGE axis in early diabetic retinopathy
    Gaetano 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)...
  38. ncbi 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...
  39. ncbi Blockade of receptor for advanced glycation endproducts: a new target for therapeutic intervention in diabetic complications and inflammatory disorders
    Barry 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...
  40. ncbi S100B-RAGE-mediated augmentation of angiotensin II-induced activation of JAK2 in vascular smooth muscle cells is dependent on PLD2
    Sean 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...
  41. ncbi The receptor RAGE as a progression factor amplifying arachidonate-dependent inflammatory and proteolytic response in human atherosclerotic plaques: role of glycemic control
    Francesco Cipollone
    University of Chieti G D Annunzio School of Medicine, Chieti, Italy
    Circulation 108:1070-7. 2003
    ..The aim of this study was to characterize RAGE expression in human plaques and to correlate it with the inflammatory infiltration, COX-2/mPGES-1 and MMP expression, and with clinical evidence of diabetes...
  42. ncbi Oral infection with a periodontal pathogen accelerates early atherosclerosis in apolipoprotein E-null mice
    Evanthia 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
    ....
  43. ncbi Receptor for AGE (RAGE) mediates neointimal formation in response to arterial injury
    Zhongmin Zhou
    Experimental Interventional Laboratory, Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA
    Circulation 107:2238-43. 2003
    ..However, the role of RAGE/ligand interaction in neointimal hyperplasia after vascular injury remains unclear...
  44. pmc Central role of RAGE-dependent neointimal expansion in arterial restenosis
    Taichi 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...
  45. pmc RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy
    Thoralf 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
    ....
  46. ncbi Suppression of experimental autoimmune encephalomyelitis by selective blockade of encephalitogenic T-cell infiltration of the central nervous system
    Shirley 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...
  47. ncbi Receptor for advanced glycation endproducts: a multiligand receptor magnifying cell stress in diverse pathologic settings
    David 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...
  48. ncbi RAGE blockade stabilizes established atherosclerosis in diabetic apolipoprotein E-null mice
    Loredana 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
    ..In this study, we tested the hypothesis that RAGE contributed to lesion progression in established atherosclerosis in diabetic apoE-null mice...
  49. ncbi Receptor for advanced glycation endproducts (RAGE) and the complications of diabetes
    David 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
    ....
  50. ncbi Receptor for advanced glycation end products on human synovial fibroblasts: role in the pathogenesis of dialysis-related amyloidosis
    Fan 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...
  51. ncbi Receptor for advanced glycation endproducts (RAGE) and vascular inflammation: insights into the pathogenesis of macrovascular complications in diabetes
    Thoralf 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...
  52. ncbi Glycation, inflammation, and RAGE: a scaffold for the macrovascular complications of diabetes and beyond
    Shi 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...
  53. ncbi Early growth response-1 promotes atherogenesis: mice deficient in early growth response-1 and apolipoprotein E display decreased atherosclerosis and vascular inflammation
    Evis 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...
  54. ncbi Aldose reductase and AGE-RAGE pathways: key players in myocardial ischemic injury
    Michiyo 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...
  55. ncbi Receptor for advanced glycation end products and its ligands: a journey from the complications of diabetes to its pathogenesis
    William 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...
  56. ncbi RAGE and amyloid beta interactions: atomic force microscopy and molecular modeling
    Michael 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...
  57. ncbi Mechanisms for the induction of HNE- MDA- and AGE-adducts, RAGE and VEGF in retinal pigment epithelial cells
    Jilin Zhou
    Department of Ophthalmology, Columbia University, 630 W 168th St, New York, NY 10032, USA
    Exp Eye Res 80:567-80. 2005
    ....
  58. ncbi Advanced glycation end products and RAGE: a common thread in aging, diabetes, neurodegeneration, and inflammation
    Ravichandran 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...
  59. ncbi Chronic vascular inflammation in patients with type 2 diabetes: endothelial biopsy and RT-PCR analysis
    Lei 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
    ....
  60. ncbi Central role of PKCbeta in neointimal expansion triggered by acute arterial injury
    Martin 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...
  61. ncbi Advanced glycation end products and vascular inflammation: implications for accelerated atherosclerosis in diabetes
    Giuseppina 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...
  62. ncbi Protein glycation: a firm link to endothelial cell dysfunction
    Jean 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...
  63. ncbi RAGE: a novel target for drug intervention in diabetic vascular disease
    Barry 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...
  64. ncbi Central role for aldose reductase pathway in myocardial ischemic injury
    Yuying 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...
  65. ncbi Enhanced expression of receptor for advanced glycation end products in chronic kidney disease
    Fan 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...
  66. ncbi RAGE axis: Animal models and novel insights into the vascular complications of diabetes
    Yoshifumi 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...
  67. ncbi Blockade of receptor for advanced glycation end product (RAGE) attenuates ischemia and reperfusion injury to the liver in mice
    Shan 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...
  68. ncbi Advanced glycation end products activate endothelium through signal-transduction receptor RAGE: a mechanism for amplification of inflammatory responses
    Giuseppina Basta
    CNR Institute of Clinical Physiology, Pisa, Italy
    Circulation 105:816-22. 2002
    ..A principal means by which AGEs alter cellular properties is through interaction with their signal-transduction receptor RAGE. We tested the hypothesis that interaction of AGEs with RAGE on endothelial cells enhances vascular activation...

Research Grants9

  1. RAGE and a Novel Tumor Axis
    Ann Schmidt; Fiscal Year: 2005
    ....