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Cardiovascular Complications in Renal Failure: Implications of Advanced Glycation End Products and Their Receptor RAGE

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Abstract

Cardiovascular disease is the major cause of death in patients with renal insufficiency, accounting for 50% of all deaths in renal replacement therapy patients and in recipients of renal transplants. Mortality from cardiovascular diseases in patients with renal failure is approximately 9% per year, which is about 30 times the risk in the general population. Evidence has emerged pointing to a potential role of oxidative stress in generation of advanced glycation end products (AGEs) in patients with end stage renal disease (ESRD). Moreover, interaction of the receptor for AGEs (RAGE) with AGEs leads to crucial biomedical pathway, generating intracellular oxidative stress and inflammatory mediators, which could result in further amplification of the pathway involved in AGE generation. AGEs and RAGE can profoundly be involved in cardiovascular diseases through regulation of (a) atherogenesis, (b) angiogenic response, (c) vascular injury, and (d) inflammatory response. Recently, numerous truncated forms of RAGE have been described, and the C-terminally truncated soluble form of RAGE has received much attention. Soluble RAGE consists of several forms including endogenous secretory RAGE (esRAGE), which is a spliced variant of RAGE, and a shedded form derived from cell surface RAGE. These heterogeneous forms of soluble RAGE, carrying all of the extracellular domains but devoid of the transmembrane and intracytoplasmic domains, bind ligands including AGEs and are capable of antagonizing RAGE signaling in vitro and in vivo. Enzyme-linked immunosorbent assay (ELISA) systems to measure plasma esRAGE and total soluble RAGE have been developed, and the pathophysiological roles of soluble RAGE have begun to be unveiled clinically. In this chapter, we will summarize the recent findings of AGEs/RAGE/soluble RAGE axis as a crucial mediator of oxidative stress and cardiovascular disease and discuss their potential usefulness as therapeutic targets and biomarkers for the disease.

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References

  1. Foley RN, Parfrey PS, Sarnak MJ. Epidemiology of cardiovascular disease in chronic renal disease. J Am Soc Nephrol 1998; 9: S16–S23.

    CAS  PubMed  Google Scholar 

  2. Lindner A, Charra B, Sherrard DJ, Scribner BH. Accelerated atherosclerosis in prolonged maintenance hemodialysis. N Engl J Med 1974; 290: 697–701.

    CAS  PubMed  Google Scholar 

  3. Stack AG, Bloembergen WE. Prevalence and clinical correlates of coronary artery disease among new dialysis patients in the United States: a cross-sectional study. J Am Soc Nephrol 2001; 12: 1516–1523.

    CAS  PubMed  Google Scholar 

  4. USRDS: the United States Renal Data System. Am J Kidney Dis 2003; 42: 1–230.

    Google Scholar 

  5. Nishimura M, Hashimoto T, Kobayashi H, Fukuda T, et al. Myocardial scintigraphy using a fatty acid analogue detects coronary artery disease in hemodialysis patients. Kidney Int 2004; 66: 811–819.

    PubMed  Google Scholar 

  6. Joki N, Hase H, Nakamura R, Yamaguchi T. Onset of coronary artery disease prior to initiation of haemodialysis in patients with end-stage renal disease. Nephrol Dial Transplant 1997; 12: 718–723.

    CAS  PubMed  Google Scholar 

  7. Ohtake T, Kobayashi S, Moriya H, Negishi K, et al. High prevalence of occult coronary artery stenosis in patients with chronic kidney disease at the initiation of renal replacement therapy: an angiographic examination. J Am Soc Nephrol 2005; 16: 1141–1148.

    PubMed  Google Scholar 

  8. Hase H, Tsunoda T, Tanaka Y, Takahashi Y, et al. Risk factors for de novo acute cardiac events in patients initiating hemodialysis with no previous cardiac symptom. Kidney Int 2006; 70: 1142–1148.

    CAS  PubMed  Google Scholar 

  9. Vanholder R, Massy Z, Argiles A, Spasovski G, et al. Chronic kidney disease as cause of cardiovascular morbidity and mortality. Nephrol Dial Transplant 2005; 20: 1048–1056.

    CAS  PubMed  Google Scholar 

  10. Hostetter TH. Chronic kidney disease predicts cardiovascular disease. N Engl J Med 2004; 351: 1344–1346.

    CAS  PubMed  Google Scholar 

  11. Redon J, Cea-Calvo L, Lozano JV, Fernandez-Perez C, et al. Kidney function and cardiovascular disease in the hypertensive population: the ERIC-HTA study. J Hypertens 2006; 24: 663–669.

    CAS  PubMed  Google Scholar 

  12. Monnier VM, Cerami A. Nonenzymatic browning in vivo: possible process for aging of long-lived proteins. Science 1981; 211: 491–493.

    CAS  PubMed  Google Scholar 

  13. Dyer DG, Blackledge JA, Thorpe SR, Baynes JW. Formation of pentosidine during nonenzymatic browning of proteins by glucose. Identification of glucose and other carbohydrates as possible precursors of pentosidine in vivo. J Biol Chem 1991; 266: 11654–11660.

    CAS  PubMed  Google Scholar 

  14. Makita Z, Radoff S, Rayfield EJ, Yang Z, et al. Advanced glycosylation end products in patients with diabetic nephropathy. N Engl J Med 1991; 325: 836–842.

    CAS  PubMed  Google Scholar 

  15. Miyata T, Ueda Y, Yoshida A, Sugiyama S, et al. Clearance of pentosidine, an advanced glycation end product, by different modalities of renal replacement therapy. Kidney Int 1997; 51: 880–887.

    CAS  PubMed  Google Scholar 

  16. Shaw S, Akyol M, Bell J, Briggs JD, et al. Effects of continuous ambulatory peritoneal dialysis and kidney transplantation on advanced glycation endproducts in the skin and peritoneum. Cell Mol Biol (Noisy-le-grand) 1998; 44: 1061–1068.

    CAS  Google Scholar 

  17. Gugliucci A, Bendayan M. Renal fate of circulating advanced glycated end products (AGE): evidence for reabsorption and catabolism of AGE-peptides by renal proximal tubular cells. Diabetologia 1996; 39: 149–160.

    CAS  PubMed  Google Scholar 

  18. Genuth S, Sun W, Cleary P, Sell DR, et al. 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. Diabetes 2005; 54: 3103–3111.

    CAS  PubMed  Google Scholar 

  19. Gerrits EG, Lutgers HL, Kleefstra N, Graaff R, et al. Skin autofluorescence: a tool to identify type 2 diabetic patients at risk for developing microvascular complications. Diabetes Care 2008; 31: 517–521.

    CAS  PubMed  Google Scholar 

  20. Sell DR, Lapolla A, Odetti P, Fogarty J, et al. Pentosidine formation in skin correlates with severity of complications in individuals with long-standing IDDM. Diabetes 1992; 41: 1286–1292.

    CAS  PubMed  Google Scholar 

  21. Friedlander MA, Wu YC, Elgawish A, Monnier VM. Early and advanced glycosylation end products. Kinetics of formation and clearance in peritoneal dialysis. J Clin Invest 1996; 97: 728–735.

    CAS  PubMed  Google Scholar 

  22. Miyata T, Fu MX, Kurokawa K, van Ypersele de Strihou C, et al. Autoxidation products of both carbohydrates and lipids are increased in uremic plasma: is there oxidative stress in uremia? Kidney Int 1998; 54: 1290–1295.

    CAS  PubMed  Google Scholar 

  23. Thorpe SR, Baynes JW. Maillard reaction products in tissue proteins: new products and new perspectives. Amino Acids 2003; 25: 275–281.

    CAS  PubMed  Google Scholar 

  24. Wolff SP, Dean RT. Glucose autoxidation and protein modification. The potential role of “autoxidative glycosylation” in diabetes. Biochem J 1987; 245: 243–250.

    CAS  PubMed  Google Scholar 

  25. Harding JJ, Beswick HT. The possible contribution of glucose autoxidation to protein modification of diabetes. Biochem J 1988; 249: 617–618.

    CAS  PubMed  Google Scholar 

  26. Miyata T, Maeda K, Kurokawa K, van Ypersele de Strihou C. Oxidation conspires with glycation to generate noxious advanced glycation end products in renal failure. Nephrol Dial Transplant 1997; 12: 255–258.

    CAS  Google Scholar 

  27. Canestrari F, Galli F, Giorgini A, Albertini MC, et al. Erythrocyte redox state in uremic anemia: effects of hemodialysis and relevance of glutathione metabolism. Acta Haematol 1994; 91: 187–193.

    CAS  PubMed  Google Scholar 

  28. Miyata T, Wada Y, Cai Z, Iida Y, et al. Implication of an increased oxidative stress in the formation of advanced glycation end products in patients with end-stage renal failure. Kidney Int 1997; 51: 1170–1181.

    CAS  PubMed  Google Scholar 

  29. Vaziri ND. Oxidative stress in uremia: nature, mechanisms, and potential consequences. Semin Nephrol 2004; 24: 469–473.

    CAS  PubMed  Google Scholar 

  30. Galli F, Varga Z, Balla J, Ferraro B, et al. Vitamin E, lipid profile, and peroxidation in hemodialysis patients. Kidney Int Suppl 2001; 78: S148–S154.

    CAS  PubMed  Google Scholar 

  31. Kosch M, Levers A, Fobker M, Barenbrock M, et al. Dialysis filter type determines the acute effect of haemodialysis on endothelial function and oxidative stress. Nephrol Dial Transplant 2003; 18: 1370–1375.

    CAS  PubMed  Google Scholar 

  32. Diepeveen SH, Verhoeven GH, van der Palen J, Dikkeschei BL, et al. Oxidative stress in patients with end-stage renal disease prior to the start of renal replacement therapy. Nephron Clin Pract 2004; 98: c3–c7.

    CAS  PubMed  Google Scholar 

  33. Witko-Sarsat V, Friedlander M, Nguyen Khoa T, Capeillere-Blandin C, et al. Advanced oxidation protein products as novel mediators of inflammation and monocyte activation in chronic renal failure. J Immunol 1998; 161: 2524–2532.

    CAS  Google Scholar 

  34. Fortuno A, Beloqui O, San Jose G, Moreno MU, et al. Increased phagocytic nicotinamide adenine dinucleotide phosphate oxidase-dependent superoxide production in patients with early chronic kidney disease. Kidney Int Suppl 2005; (99): S71–S75.

    Google Scholar 

  35. Yilmaz MI, Saglam M, Caglar K, Cakir E, et al. The determinants of endothelial dysfunction in CKD: oxidative stress and asymmetric dimethylarginine. Am J Kidney Dis 2006; 47: 42–50.

    CAS  PubMed  Google Scholar 

  36. Ceballos-Picot I, Witko-Sarsat V, Merad-Boudia M, Nguyen AT, et al. Glutathione antioxidant system as a marker of oxidative stress in chronic renal failure. Free Radic Biol Med 1996; 21: 845–853.

    CAS  PubMed  Google Scholar 

  37. Niwa T. 3-Deoxyglucosone: metabolism, analysis, biological activity, and clinical implication. J Chromatogr B Biomed Sci Appl 1999; 731: 23–36.

    CAS  PubMed  Google Scholar 

  38. Williamson JR, Chang K, Frangos M, Hasan KS, et al. Hyperglycemic pseudohypoxia and diabetic complications. Diabetes 1993; 42: 801–813.

    CAS  PubMed  Google Scholar 

  39. Thornalley PJ. Glyoxalase I – structure, function and a critical role in the enzymatic defence against glycation. Biochem Soc Trans 2003; 31: 1343–1348.

    CAS  PubMed  Google Scholar 

  40. Miyata T, van Ypersele de Strihou C, Imasawa T, Yoshino A, et al. Glyoxalase I deficiency is associated with an unusual level of advanced glycation end products in a hemodialysis patient. Kidney Int 2001; 60: 2351–2359.

    CAS  Google Scholar 

  41. Waanders F, Greven WL, Baynes JW, Thorpe SR, et al. Renal accumulation of pentosidine in non-diabetic proteinuria-induced renal damage in rats. Nephrol Dial Transplant 2005; 20: 2060–2070.

    CAS  PubMed  Google Scholar 

  42. Koschinsky T, He CJ, Mitsuhashi T, Bucala R, et al. Orally absorbed reactive glycation products (glycotoxins): an environmental risk factor in diabetic nephropathy. Proc Natl Acad Sci USA 1997; 94: 6474–6479.

    CAS  PubMed  Google Scholar 

  43. Cerami C, Founds H, Nicholl I, Mitsuhashi T, et al. Tobacco smoke is a source of toxic reactive glycation products. Proc Natl Acad Sci U S A 1997; 94: 13915–13920.

    CAS  PubMed  Google Scholar 

  44. DeFronzo RA, Alvestrand A, Smith D, Hendler R, et al. Insulin resistance in uremia. J Clin Invest 1981; 67: 563–568.

    CAS  PubMed  Google Scholar 

  45. Park K, Gross M, Lee DH, Holvoet P, et al. Oxidative stress and insulin resistance: the coronary artery risk development in young adults study. Diabetes Care 2009; 32: 1302–1307.

    CAS  PubMed  Google Scholar 

  46. Sakata N, Imanaga Y, Meng J, Tachikawa Y, et al. Increased advanced glycation end products in atherosclerotic lesions of patients with end-stage renal disease. Atherosclerosis 1999; 142: 67–77.

    CAS  PubMed  Google Scholar 

  47. Yoshida S, Yamada K, Hamaguchi K, Nishimura M, et al. Immunohistochemical study of human advanced glycation end-products (AGE) and growth factors in cardiac tissues of patients on maintenance dialysis and with kidney transplantation. Clin Nephrol 1998; 49: 273–280.

    CAS  PubMed  Google Scholar 

  48. Bucala R, Makita Z, Vega G, Grundy S, et al. Modification of low density lipoprotein by advanced glycation end products contributes to the dyslipidemia of diabetes and renal insufficiency. Proc Natl Acad Sci U S A 1994; 91: 9441–9445.

    CAS  PubMed  Google Scholar 

  49. Oranje WA, Wolffenbuttel BH. Lipid peroxidation and atherosclerosis in type II diabetes. J Lab Clin Med 1999; 134: 19–32.

    CAS  PubMed  Google Scholar 

  50. Drueke TB, Nguyen Khoa T, Massy ZA, Witko-Sarsat V, et al. Role of oxidized low-density lipoprotein in the atherosclerosis of uremia. Kidney Int Suppl 2001; 78: S114–S119.

    CAS  PubMed  Google Scholar 

  51. Stocker R, Keaney JF, Jr. Role of oxidative modifications in atherosclerosis. Physiol Rev 2004; 84: 1381–1478.

    CAS  PubMed  Google Scholar 

  52. Suliman ME, Stenvinkel P, Jogestrand T, Maruyama Y, et al. Plasma pentosidine and total homocysteine levels in relation to change in common carotid intima-media area in the first year of dialysis therapy. Clin Nephrol 2006; 66: 418–425.

    CAS  PubMed  Google Scholar 

  53. Taki K, Takayama F, Tsuruta Y, Niwa T. Oxidative stress, advanced glycation end product, and coronary artery calcification in hemodialysis patients. Kidney Int 2006; 70: 218–224.

    CAS  PubMed  Google Scholar 

  54. Tarsio JF, Reger LA, Furcht LT. Decreased interaction of fibronectin, type IV collagen, and heparin due to nonenzymatic glycation. Implications for diabetes mellitus. Biochemistry 1987; 26: 1014–1020.

    CAS  Google Scholar 

  55. Klein DJ, Oegema TR, Jr., Brown DM. Release of glomerular heparan-35SO4 proteoglycan by heparin from glomeruli of streptozocin-induced diabetic rats. Diabetes 1989; 38: 130–139.

    CAS  PubMed  Google Scholar 

  56. Blacher J, Guerin AP, Pannier B, Marchais SJ, et al. Impact of aortic stiffness on survival in end-stage renal disease. Circulation 1999; 99: 2434–2439.

    CAS  PubMed  Google Scholar 

  57. Shoji T, Emoto M, Shinohara K, Kakiya R, et al. Diabetes mellitus, aortic stiffness, and cardiovascular mortality in end-stage renal disease. J Am Soc Nephrol 2001; 12: 2117–2124.

    CAS  PubMed  Google Scholar 

  58. Kitahara T, Ono K, Tsuchida A, Kawai H, et al. Impact of brachial-ankle pulse wave velocity and ankle-brachial blood pressure index on mortality in hemodialysis patients. Am J Kidney Dis 2005; 46: 688–696.

    PubMed  Google Scholar 

  59. Meerwaldt R, Graaff R, Oomen PH, Links TP, et al. Simple non-invasive assessment of advanced glycation endproduct accumulation. Diabetologia 2004; 47: 1324–1330.

    CAS  PubMed  Google Scholar 

  60. Ueno H, Koyama H, Tanaka S, Fukumoto S, et al. Skin autofluorescence, a marker for advanced glycation end product accumulation, is associated with arterial stiffness in patients with end-stage renal disease. Metabolism 2008; 57: 1452–1457.

    CAS  PubMed  Google Scholar 

  61. Wolffenbuttel BH, Boulanger CM, Crijns FR, Huijberts MS, et al. Breakers of advanced glycation end products restore large artery properties in experimental diabetes. Proc Natl Acad Sci USA 1998; 95: 4630–4634.

    CAS  PubMed  Google Scholar 

  62. Kass DA, Shapiro EP, Kawaguchi M, Capriotti AR, et al. Improved arterial compliance by a novel advanced glycation end-product crosslink breaker. Circulation 2001; 104: 1464–1470.

    CAS  PubMed  Google Scholar 

  63. Meerwaldt R, Hartog JW, Graaff R, Huisman RJ, et al. Skin autofluorescence, a measure of cumulative metabolic stress and advanced glycation end products, predicts mortality in hemodialysis patients. J Am Soc Nephrol 2005; 16: 3687–3693.

    CAS  PubMed  Google Scholar 

  64. Meerwaldt R, Lutgers HL, Links TP, Graaff R, et al. Skin autofluorescence is a strong predictor of cardiac mortality in diabetes. Diabetes Care 2007; 30: 107–112.

    CAS  PubMed  Google Scholar 

  65. Roberts MA, Thomas MC, Fernando D, Macmillan N, et al. Low molecular weight advanced glycation end products predict mortality in asymptomatic patients receiving chronic haemodialysis. Nephrol Dial Transplant 2006; 21: 1611–1617.

    CAS  PubMed  Google Scholar 

  66. Wagner Z, Molnar M, Molnar GA, Tamasko M, et al. Serum carboxymethyllysine predicts mortality in hemodialysis patients. Am J Kidney Dis 2006; 47: 294–300.

    CAS  PubMed  Google Scholar 

  67. Schwedler SB, Metzger T, Schinzel R, Wanner C. Advanced glycation end products and mortality in hemodialysis patients. Kidney Int 2002; 62: 301–310.

    CAS  PubMed  Google Scholar 

  68. Busch M, Franke S, Muller A, Wolf M, et al. Potential cardiovascular risk factors in chronic kidney disease: AGEs, total homocysteine and metabolites, and the C-reactive protein. Kidney Int 2004; 66: 338–347.

    CAS  PubMed  Google Scholar 

  69. Pecoits-Filho R, Lindholm B, Stenvinkel P. The malnutrition, inflammation, and atherosclerosis (MIA) syndrome – the heart of the matter. Nephrol Dial Transplant 2002; 17:(Suppl 11): 28–31.

    CAS  PubMed  Google Scholar 

  70. Rambod M, Bross R, Zitterkoph J, Benner D, et al. Association of Malnutrition-Inflammation Score with quality of life and mortality in hemodialysis patients: a 5-year prospective cohort study. Am J Kidney Dis 2009; 53: 298–309.

    PubMed  Google Scholar 

  71. Schmidt AM, Vianna M, Gerlach M, Brett J, et al. Isolation and characterization of two binding proteins for advanced glycosylation end products from bovine lung which are present on the endothelial cell surface. J Biol Chem 1992; 267: 14987–14997.

    CAS  PubMed  Google Scholar 

  72. Neeper M, Schmidt AM, Brett J, Yan SD, et al. Cloning and expression of a cell surface receptor for advanced glycosylation end products of proteins. J Biol Chem 1992; 267: 14998–15004.

    CAS  PubMed  Google Scholar 

  73. Kislinger T, Fu C, Huber B, Qu W, et al. N(epsilon)-(carboxymethyl)lysine adducts of proteins are ligands for receptor for advanced glycation end products that activate cell signaling pathways and modulate gene expression. J Biol Chem 1999; 274: 31740–31749.

    CAS  PubMed  Google Scholar 

  74. Reddy S, Bichler J, Wells-Knecht KJ, Thorpe SR, et al. N epsilon-(carboxymethyl)lysine is a dominant advanced glycation end product (AGE) antigen in tissue proteins. Biochemistry 1995; 34: 10872–10878.

    CAS  PubMed  Google Scholar 

  75. Xie J, Reverdatto S, Frolov A, Hoffmann R, et al. Structural basis for pattern recognition by the receptor for advanced glycation end products (RAGE). J Biol Chem 2008; 283: 27255–27269.

    CAS  PubMed  Google Scholar 

  76. Matsumoto S, Yoshida T, Murata H, Harada S, et al. Solution structure of the variable-type domain of the receptor for advanced glycation end products: new insight into AGE-RAGE interaction. Biochemistry 2008; 47: 12299–12311.

    CAS  PubMed  Google Scholar 

  77. Hofmann MA, Drury S, Fu C, Qu W, et al. RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides. Cell 1999; 97: 889–901.

    CAS  PubMed  Google Scholar 

  78. Hori O, Brett J, Slattery T, Cao R, et al. The receptor for advanced glycation end products (RAGE) is a cellular binding site for amphoterin. Mediation of neurite outgrowth and co-expression of rage and amphoterin in the developing nervous system. J Biol Chem 1995; 270: 25752–25761.

    CAS  Google Scholar 

  79. Taguchi A, Blood DC, del Toro G, Canet A, et al. Blockade of RAGE-amphoterin signalling suppresses tumour growth and metastases. Nature 2000; 405: 354–360.

    CAS  PubMed  Google Scholar 

  80. Yan SD, Chen X, Fu J, Chen M, et al. RAGE and amyloid-beta peptide neurotoxicity in Alzheimer’s disease. Nature 1996; 382: 685–691.

    CAS  PubMed  Google Scholar 

  81. Sousa MM, Yan SD, Stern D, Saraiva MJ. Interaction of the receptor for advanced glycation end products (RAGE) with transthyretin triggers nuclear transcription factor κB (NF-κB) activation. Lab Invest 2000; 80: 1101–1110.

    CAS  PubMed  Google Scholar 

  82. Chavakis T, Bierhaus A, Al-Fakhri N, Schneider D, et al. The pattern recognition receptor (RAGE) is a counterreceptor for leukocyte integrins: a novel pathway for inflammatory cell recruitment. J Exp Med 2003; 198: 1507–1515.

    CAS  PubMed  Google Scholar 

  83. Krieger M, Stern DM. Series introduction: multiligand receptors and human disease. J Clin Invest 2001; 108: 645–647.

    CAS  PubMed  Google Scholar 

  84. Schmidt AM, Yan SD, Yan SF, Stern DM. The multiligand receptor RAGE as a progression factor amplifying immune and inflammatory responses. J Clin Invest 2001; 108: 949–955.

    CAS  PubMed  Google Scholar 

  85. Yamamoto Y, Kato I, Doi T, Yonekura H, et al. Development and prevention of advanced diabetic nephropathy in RAGE-overexpressing mice. J Clin Invest 2001; 108: 261–268.

    CAS  PubMed  Google Scholar 

  86. Myint KM, Yamamoto Y, Doi T, Kato I, et al. RAGE control of diabetic nephropathy in a mouse model: effects of RAGE gene disruption and administration of low-molecular weight heparin. Diabetes 2006; 55: 2510–2522.

    CAS  PubMed  Google Scholar 

  87. Bierhaus A, Haslbeck KM, Humpert PM, Liliensiek B, et al. Loss of pain perception in diabetes is dependent on a receptor of the immunoglobulin superfamily. J Clin Invest 2004; 114: 1741–1751.

    CAS  PubMed  Google Scholar 

  88. Toth C, Rong LL, Yang C, Martinez J, et al. Receptor for advanced glycation end products (RAGEs) and experimental diabetic neuropathy. Diabetes 2008; 57: 1002–1017.

    CAS  PubMed  Google Scholar 

  89. Xu D, Kyriakis JM. Phosphatidylinositol 3’-kinase-dependent activation of renal mesangial cell Ki-Ras and ERK by advanced glycation end products. J Biol Chem 2003; 278: 39349–39355.

    CAS  PubMed  Google Scholar 

  90. Yan SD, Schmidt AM, Anderson GM, Zhang J, et al. Enhanced cellular oxidant stress by the interaction of advanced glycation end products with their receptors/binding proteins. J Biol Chem 1994; 269: 9889–9897.

    CAS  PubMed  Google Scholar 

  91. Wautier MP, Chappey O, Corda S, Stern DM, et al. Activation of NADPH oxidase by AGE links oxidant stress to altered gene expression via RAGE. Am J Physiol Endocrinol Metab 2001; 280: E685–E694.

    CAS  PubMed  Google Scholar 

  92. Dukic-Stefanovic S, Gasic-Milenkovic J, Deuther-Conrad W, Munch G. Signal transduction pathways in mouse microglia N-11 cells activated by advanced glycation endproducts (AGEs). J Neurochem 2003; 87: 44–55.

    CAS  PubMed  Google Scholar 

  93. Li J, Schmidt AM. Characterization and functional analysis of the promoter of RAGE, the receptor for advanced glycation end products. J Biol Chem 1997; 272: 16498–16506.

    CAS  PubMed  Google Scholar 

  94. Bierhaus A, Schiekofer S, Schwaninger M, Andrassy M, et al. Diabetes-associated sustained activation of the transcription factor nuclear factor-kappaB. Diabetes 2001; 50: 2792–2808.

    CAS  PubMed  Google Scholar 

  95. Shanmugam N, Kim YS, Lanting L, Natarajan R. Regulation of cyclooxygenase-2 expression in monocytes by ligation of the receptor for advanced glycation end products. J Biol Chem 2003; 278: 34834–34844.

    CAS  PubMed  Google Scholar 

  96. Schmidt AM, Hori O, Chen JX, Li JF, et al. 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. J Clin Invest 1995; 96: 1395–1403.

    CAS  PubMed  Google Scholar 

  97. Vlassara H. The AGE-receptor in the pathogenesis of diabetic complications. Diabetes Metab Res Rev 2001; 17: 436–443.

    CAS  PubMed  Google Scholar 

  98. Basta G, Lazzerini G, Massaro M, Simoncini T, et al. Advanced glycation end products activate endothelium through signal-transduction receptor RAGE: a mechanism for amplification of inflammatory responses. Circulation 2002; 105: 816–822.

    CAS  PubMed  Google Scholar 

  99. Hou FF, Ren H, Owen WF, Jr, Guo ZJ, et al. Enhanced expression of receptor for advanced glycation end products in chronic kidney disease. J Am Soc Nephrol 2004; 15: 1889–1896.

    CAS  PubMed  Google Scholar 

  100. Rodriguez-Ayala E, Anderstam B, Suliman ME, Seeberger A, et al. Enhanced RAGE-mediated NFkappaB stimulation in inflamed hemodialysis patients. Atherosclerosis 2005; 180: 333–340.

    CAS  PubMed  Google Scholar 

  101. Linden E, Cai W, He JC, Xue C, et al. Endothelial dysfunction in patients with chronic kidney disease results from advanced glycation end products (AGE)-mediated inhibition of endothelial nitric oxide synthase through RAGE activation. Clin J Am Soc Nephrol 2008; 3: 691–698.

    CAS  PubMed  Google Scholar 

  102. Greten J, Kreis I, Wiesel K, Stier E, et al. Receptors for advance glycation end-products (AGE) – expression by endothelial cells in non-diabetic uraemic patients. Nephrol Dial Transplant 1996; 11: 786–790.

    CAS  PubMed  Google Scholar 

  103. Kawagishi T, Nishizawa Y, Konishi T, Kawasaki K, et al. High-resolution B-mode ultrasonography in evaluation of atherosclerosis in uremia. Kidney Int 1995; 48: 820–826.

    CAS  PubMed  Google Scholar 

  104. Cipollone F, Iezzi A, Fazia M, Zucchelli M, et al. The receptor RAGE as a progression factor amplifying arachidonate-dependent inflammatory and proteolytic response in human atherosclerotic plaques: role of glycemic control. Circulation 2003; 108: 1070–1077.

    CAS  PubMed  Google Scholar 

  105. Burke AP, Kolodgie FD, Zieske A, Fowler DR, et al. Morphologic findings of coronary atherosclerotic plaques in diabetics: a postmortem study. Arterioscler Thromb Vasc Biol 2004; 24: 1266–1271.

    CAS  PubMed  Google Scholar 

  106. Park L, Raman KG, Lee KJ, Lu Y, et al. Suppression of accelerated diabetic atherosclerosis by the soluble receptor for advanced glycation endproducts. Nat Med 1998; 4: 1025–1031.

    CAS  PubMed  Google Scholar 

  107. Kislinger T, Tanji N, Wendt T, Qu W, et al. Receptor for advanced glycation end products mediates inflammation and enhanced expression of tissue factor in vasculature of diabetic apolipoprotein E-null mice. Arterioscler Thromb Vasc Biol 2001; 21: 905–910.

    CAS  PubMed  Google Scholar 

  108. Wendt T, Harja E, Bucciarelli L, Qu W, et al. RAGE modulates vascular inflammation and atherosclerosis in a murine model of type 2 diabetes. Atherosclerosis 2006; 185: 70–77.

    CAS  PubMed  Google Scholar 

  109. Bucciarelli LG, Wendt T, Qu W, Lu Y, et al. RAGE blockade stabilizes established atherosclerosis in diabetic apolipoprotein E-null mice. Circulation 2002; 106: 2827–2835.

    CAS  PubMed  Google Scholar 

  110. Soro-Paavonen A, Watson AM, Li J, Paavonen K, et al. Receptor for advanced glycation end products (RAGE) deficiency attenuates the development of atherosclerosis in diabetes. Diabetes 2008; 57: 2461–2469.

    CAS  PubMed  Google Scholar 

  111. Harja E, Bu DX, Hudson BI, Chang JS, et al. Vascular and inflammatory stresses mediate atherosclerosis via RAGE and its ligands in apoE-/- mice. J Clin Invest 2008; 118: 183–194.

    CAS  PubMed  Google Scholar 

  112. Massy ZA, Ivanovski O, Nguyen-Khoa T, Angulo J, et al. Uremia accelerates both atherosclerosis and arterial calcification in apolipoprotein E knockout mice. J Am Soc Nephrol 2005; 16: 109–116.

    CAS  PubMed  Google Scholar 

  113. Phan O, Ivanovski O, Nguyen-Khoa T, Mothu N, et al. Sevelamer prevents uremia-enhanced atherosclerosis progression in apolipoprotein E-deficient mice. Circulation 2005; 112: 2875–2882.

    CAS  PubMed  Google Scholar 

  114. Bro S, Flyvbjerg A, Binder CJ, Bang CA, et al. A neutralizing antibody against receptor for advanced glycation end products (RAGE) reduces atherosclerosis in uremic mice. Atherosclerosis 2008; 201: 274–280.

    CAS  PubMed  Google Scholar 

  115. Mizutani M, Kern TS, Lorenzi M. Accelerated death of retinal microvascular cells in human and experimental diabetic retinopathy. J Clin Invest 1996; 97: 2883–2890.

    CAS  PubMed  Google Scholar 

  116. Stitt A, Gardiner TA, Anderson NL, Canning P, et al. The AGE inhibitor pyridoxamine inhibits development of retinopathy in experimental diabetes. Diabetes 2002; 51: 2826–2832.

    CAS  PubMed  Google Scholar 

  117. Hammes HP, Du X, Edelstein D, Taguchi T, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy. Nat Med 2003; 9: 294–299.

    CAS  PubMed  Google Scholar 

  118. Abaci A, Oguzhan A, Kahraman S, Eryol NK, et al. Effect of diabetes mellitus on formation of coronary collateral vessels. Circulation 1999; 99: 2239–2242.

    CAS  PubMed  Google Scholar 

  119. Rivard A, Silver M, Chen D, Kearney M, et al. Rescue of diabetes-related impairment of angiogenesis by intramuscular gene therapy with adeno-VEGF. Am J Pathol 1999; 154: 355–363.

    CAS  PubMed  Google Scholar 

  120. Waltenberger J. Impaired collateral vessel development in diabetes: potential cellular mechanisms and therapeutic implications. Cardiovasc Res 2001; 49: 554–560.

    CAS  PubMed  Google Scholar 

  121. Stitt AW, McGoldrick C, Rice-McCaldin A, McCance DR, et al. Impaired retinal angiogenesis in diabetes: role of advanced glycation end products and galectin-3. Diabetes 2005; 54: 785–794.

    CAS  PubMed  Google Scholar 

  122. Goova MT, Li J, Kislinger T, Qu W, et al. Blockade of receptor for advanced glycation end-products restores effective wound healing in diabetic mice. Am J Pathol 2001; 159: 513–525.

    CAS  PubMed  Google Scholar 

  123. Tamarat R, Silvestre JS, Huijberts M, Benessiano J, et al. Blockade of advanced glycation end-product formation restores ischemia-induced angiogenesis in diabetic mice. Proc Natl Acad Sci USA 2003; 100: 8555–8560.

    CAS  PubMed  Google Scholar 

  124. Shoji T, Koyama H, Morioka T, Tanaka S, et al. Receptor for advanced glycation end products is involved in impaired angiogenic response in diabetes. Diabetes 2006; 55: 2245–2255.

    CAS  PubMed  Google Scholar 

  125. Koyama H, Yamamoto H, Nishizawa Y. RAGE and soluble RAGE: potential therapeutic targets for cardiovascular diseases. Mol Med 2007; 13: 625–635.

    CAS  PubMed  Google Scholar 

  126. Asahara T, Murohara T, Sullivan A, Silver M, et al. Isolation of putative progenitor endothelial cells for angiogenesis. Science 1997; 275: 964–967.

    CAS  PubMed  Google Scholar 

  127. Rafii S, Lyden D. Therapeutic stem and progenitor cell transplantation for organ vascularization and regeneration. Nat Med 2003; 9: 702–712.

    CAS  PubMed  Google Scholar 

  128. Rauscher FM, Goldschmidt-Clermont PJ, Davis BH, Wang T, et al. Aging, progenitor cell exhaustion, and atherosclerosis. Circulation 2003; 108: 457–463.

    PubMed  Google Scholar 

  129. Choi JH, Kim KL, Huh W, Kim B, et al. Decreased number and impaired angiogenic function of endothelial progenitor cells in patients with chronic renal failure. Arterioscler Thromb Vasc Biol 2004; 24: 1246–1252.

    CAS  PubMed  Google Scholar 

  130. de Groot K, Bahlmann FH, Sowa J, Koenig J, et al. Uremia causes endothelial progenitor cell deficiency. Kidney Int 2004; 66: 641–646.

    PubMed  Google Scholar 

  131. Herbrig K, Pistrosch F, Oelschlaegel U, Wichmann G, et al. Increased total number but impaired migratory activity and adhesion of endothelial progenitor cells in patients on long-term hemodialysis. Am J Kidney Dis 2004; 44: 840–849.

    PubMed  Google Scholar 

  132. Schlieper G, Hristov M, Brandenburg V, Kruger T, et al. Predictors of low circulating endothelial progenitor cell numbers in haemodialysis patients. Nephrol Dial Transplant 2008; 23: 2611–2618.

    PubMed  Google Scholar 

  133. Ueno H, Koyama H, Fukumoto S, Tanaka S, et al. Dialysis modality is independently associated with circulating endothelial progenitor cells in end-stage renal diseases patients. Nephrol Dial Transplant 2010; 25: 581–586.

    CAS  PubMed  Google Scholar 

  134. Tepper OM, Galiano RD, Capla JM, Kalka C, et al. Human endothelial progenitor cells from type II diabetics exhibit impaired proliferation, adhesion, and incorporation into vascular structures. Circulation 2002; 106: 2781–2786.

    PubMed  Google Scholar 

  135. Fadini GP, Sartore S, Agostini C, Avogaro A. Significance of endothelial progenitor cells in subjects with diabetes. Diabetes Care 2007; 30: 1305–1313.

    CAS  PubMed  Google Scholar 

  136. Scheubel RJ, Zorn H, Silber RE, Kuss O, et al. Age-dependent depression in circulating endothelial progenitor cells in patients undergoing coronary artery bypass grafting. J Am Coll Cardiol 2003; 42: 2073–2080.

    PubMed  Google Scholar 

  137. Heiss C, Keymel S, Niesler U, Ziemann J, et al. Impaired progenitor cell activity in age-related endothelial dysfunction. J Am Coll Cardiol 2005; 45: 1441–1448.

    CAS  PubMed  Google Scholar 

  138. Ueno H, Koyama H, Fukumoto S, Tanaka S, et al. Advanced glycation end-products, carotid atherosclerosis and circulating endothelial progenitor cells in patients with end-stage renal disease. Metabolism 2010 in press

    Google Scholar 

  139. Chavakis E, Hain A, Vinci M, Carmona G, et al. High-mobility group box1 activates integrin-dependent homing of endothelial progenitor cells. Circ Res 2007; 100: 204–212.

    CAS  PubMed  Google Scholar 

  140. Kahn JK, Rutherford BD, McConahay DR, Johnson WL, et al. Short- and long-term outcome of percutaneous transluminal coronary angioplasty in chronic dialysis patients. Am Heart J 1990; 119: 484–489.

    CAS  PubMed  Google Scholar 

  141. Ahmed WH, Shubrooks SJ, Gibson CM, Baim DS, et al. Complications and long-term outcome after percutaneous coronary angioplasty in chronic hemodialysis patients. Am Heart J 1994; 128: 252–255.

    CAS  PubMed  Google Scholar 

  142. Azar RR, Prpic R, Ho KK, Kiernan FJ, et al. Impact of end-stage renal disease on clinical and angiographic outcomes after coronary stenting. Am J Cardiol 2000; 86: 485–489.

    CAS  PubMed  Google Scholar 

  143. Rozenman Y, Sapoznikov D, Mosseri M, Gilon D, et al. Long-term angiographic follow-up of coronary balloon angioplasty in patients with diabetes mellitus: a clue to the explanation of the results of the BARI study. Balloon Angioplasty Revascularization Investigation. J Am Coll Cardiol 1997; 30: 1420–1425.

    CAS  Google Scholar 

  144. Abizaid A, Kornowski R, Mintz GS, Hong MK, et al. The influence of diabetes mellitus on acute and late clinical outcomes following coronary stent implantation. J Am Coll Cardiol 1998; 32: 584–589.

    CAS  PubMed  Google Scholar 

  145. Zhou Z, Wang K, Penn MS, Marso SP, et al. Receptor for AGE (RAGE) mediates neointimal formation in response to arterial injury. Circulation 2003; 107: 2238–2243.

    CAS  PubMed  Google Scholar 

  146. Sakaguchi T, Yan SF, Yan SD, Belov D, et al. Central role of RAGE-dependent neointimal expansion in arterial restenosis. J Clin Invest 2003; 111: 959–972.

    CAS  PubMed  Google Scholar 

  147. Ross R. Atherosclerosis – an inflammatory disease. N Engl J Med 1999; 340: 115–126.

    CAS  PubMed  Google Scholar 

  148. Schmidt AM, Yan SD, Brett J, Mora R, et al. Regulation of human mononuclear phagocyte migration by cell surface-binding proteins for advanced glycation end products. J Clin Invest 1993; 91: 2155–2168.

    CAS  PubMed  Google Scholar 

  149. Rouhiainen A, Kuja-Panula J, Wilkman E, Pakkanen J, et al. Regulation of monocyte migration by amphoterin (HMGB1). Blood 2004; 104: 1174–1182.

    CAS  PubMed  Google Scholar 

  150. Yan SS, Wu ZY, Zhang HP, Furtado G, et al. Suppression of experimental autoimmune encephalomyelitis by selective blockade of encephalitogenic T-cell infiltration of the central nervous system. Nat Med 2003; 9: 287–293.

    CAS  PubMed  Google Scholar 

  151. Chen Y, Yan SS, Colgan J, Zhang HP, et al. Blockade of late stages of autoimmune diabetes by inhibition of the receptor for advanced glycation end products. J Immunol 2004; 173: 1399–1405.

    CAS  PubMed  Google Scholar 

  152. Moser B, Szabolcs MJ, Ankersmit HJ, Lu Y, et al. Blockade of RAGE suppresses alloimmune reactions in vitro and delays allograft rejection in murine heart transplantation. Am J Transplant 2007; 7: 293–302.

    CAS  PubMed  Google Scholar 

  153. Tian J, Avalos AM, Mao SY, Chen B, et al. Toll-like receptor 9-dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE. Nat Immunol 2007; 8: 487–496.

    CAS  PubMed  Google Scholar 

  154. Orlova VV, Choi EY, Xie C, Chavakis E, et al. A novel pathway of HMGB1-mediated inflammatory cell recruitment that requires Mac-1-integrin. Embo J 2007; 26: 1129–1139.

    CAS  PubMed  Google Scholar 

  155. Malherbe P, Richards JG, Gaillard H, Thompson A, et al. cDNA cloning of a novel secreted isoform of the human receptor for advanced glycation end products and characterization of cells co-expressing cell-surface scavenger receptors and Swedish mutant amyloid precursor protein. Brain Res Mol Brain Res 1999; 71: 159–170.

    CAS  PubMed  Google Scholar 

  156. Yonekura H, Yamamoto Y, Sakurai S, Petrova RG, et al. Novel splice variants of the receptor for advanced glycation end-products expressed in human vascular endothelial cells and pericytes, and their putative roles in diabetes-induced vascular injury. Biochem J 2003; 370: 1097–1109.

    CAS  PubMed  Google Scholar 

  157. Schlueter C, Hauke S, Flohr AM, Rogalla P, et al. Tissue-specific expression patterns of the RAGE receptor and its soluble forms – a result of regulated alternative splicing? Biochim Biophys Acta 2003; 1630: 1–6.

    CAS  PubMed  Google Scholar 

  158. Park IH, Yeon SI, Youn JH, Choi JE, et al. Expression of a novel secreted splice variant of the receptor for advanced glycation end products (RAGE) in human brain astrocytes and peripheral blood mononuclear cells. Mol Immunol 2004; 40: 1203–1211.

    CAS  PubMed  Google Scholar 

  159. Ding Q, Keller JN. Splice variants of the receptor for advanced glycosylation end products (RAGE) in human brain. Neurosci Lett 2005; 373: 67–72.

    CAS  PubMed  Google Scholar 

  160. Hudson BI, Carter AM, Harja E, Kalea AZ, et al. Identification, classification, and expression of RAGE gene splice variants. FASEB J 2008; 22: 1572–1580.

    CAS  PubMed  Google Scholar 

  161. Kalea AZ, Reiniger N, Yang H, Arriero M, et al. Alternative splicing of the murine receptor for advanced glycation end-products (RAGE) gene. FASEB J 2009; 23: 1766–1774.

    CAS  PubMed  Google Scholar 

  162. Bierhaus A, Humpert PM, Morcos M, Wendt T, et al. Understanding RAGE, the receptor for advanced glycation end products. J Mol Med 2005; 83: 876–886.

    CAS  PubMed  Google Scholar 

  163. Hudson BI, Harja E, Moser B, Schmidt AM. Soluble levels of receptor for advanced glycation endproducts (sRAGE) and coronary artery disease: the next C-reactive protein? Arterioscler Thromb Vasc Biol 2005; 25: 879–882.

    CAS  PubMed  Google Scholar 

  164. Hanford LE, Enghild JJ, Valnickova Z, Petersen SV, et al. Purification and characterization of mouse soluble receptor for advanced glycation end products (sRAGE). J Biol Chem 2004; 279: 50019–50024.

    CAS  PubMed  Google Scholar 

  165. Raucci A, Cugusi S, Antonelli A, Barabino SM, et al. A soluble form of the receptor for advanced glycation endproducts (RAGE) is produced by proteolytic cleavage of the membrane-bound form by the sheddase a disintegrin and metalloprotease 10 (ADAM10). FASEB J 2008; 22: 3716–3727.

    CAS  PubMed  Google Scholar 

  166. Zhang L, Bukulin M, Kojro E, Roth A, et al. Receptor for advanced glycation end products is subjected to protein ectodomain shedding by metalloproteinases. J Biol Chem 2008; 283: 35507–35516.

    CAS  PubMed  Google Scholar 

  167. Pullerits R, Brisslert M, Jonsson IM, Tarkowski A. Soluble receptor for advanced glycation end products triggers a proinflammatory cytokine cascade via beta2 integrin Mac-1. Arthritis Rheum 2006; 54: 3898–3907.

    CAS  PubMed  Google Scholar 

  168. Falcone C, Emanuele E, D’Angelo A, Buzzi MP, et al. Plasma levels of soluble receptor for advanced glycation end products and coronary artery disease in nondiabetic men. Arterioscler Thromb Vasc Biol 2005; 25: 1032–1037.

    CAS  PubMed  Google Scholar 

  169. Emanuele E, D’Angelo A, Tomaino C, Binetti G, et al. Circulating levels of soluble receptor for advanced glycation end products in Alzheimer disease and vascular dementia. Arch Neurol 2005; 62: 1734–1736.

    PubMed  Google Scholar 

  170. Sakurai S, Yamamoto Y, Tamei H, Matsuki H, et al. Development of an ELISA for esRAGE and its application to type 1 diabetic patients. Diabetes Res Clin Pract 2006; 73: 158–165.

    CAS  PubMed  Google Scholar 

  171. Koyama H, Shoji T, Yokoyama H, Motoyama K, et al. Plasma level of endogenous secretory RAGE is associated with components of the metabolic syndrome and atherosclerosis. Arterioscler Thromb Vasc Biol 2005; 25: 2587–2593.

    CAS  PubMed  Google Scholar 

  172. Nakamura K, Yamagishi S, Adachi H, Kurita-Nakamura Y, et al. Elevation of soluble form of receptor for advanced glycation end products (sRAGE) in diabetic subjects with coronary artery disease. Diabetes Metab Res Rev 2007; 23: 368–371.

    CAS  PubMed  Google Scholar 

  173. Nin JW, Ferreira I, Schalkwijk CG, Prins MH, et al. Levels of soluble receptor for AGE are cross-sectionally associated with cardiovascular disease in type 1 diabetes, and this association is partially mediated by endothelial and renal dysfunction and by low-grade inflammation: the EURODIAB prospective complications study. Diabetologia 2009; 52: 705–714.

    CAS  PubMed  Google Scholar 

  174. Katakami N, Matsuhisa M, Kaneto H, Matsuoka TA, et al. Decreased endogenous secretory advanced glycation end product receptor in type 1 diabetic patients: its possible association with diabetic vascular complications. Diabetes Care 2005; 28: 2716–2721.

    CAS  PubMed  Google Scholar 

  175. Katakami N, Matsuhisa M, Kaneto H, Matsuoka TA, et al. Endogenous secretory RAGE but not soluble RAGE is associated with carotid atherosclerosis in type 1 diabetes patients. Diab Vasc Dis Res 2008; 5: 190–197.

    PubMed  Google Scholar 

  176. Katakami N, Matsuhisa M, Kaneto H, Yamasaki Y. Serum endogenous secretory RAGE levels are inversely associated with carotid IMT in type 2 diabetic patients. Atherosclerosis 2007; 190: 22–23.

    CAS  PubMed  Google Scholar 

  177. Humpert PM, Djuric Z, Kopf S, Rudofsky G, et al. Soluble RAGE but not endogenous secretory RAGE is associated with albuminuria in patients with type 2 diabetes. Cardiovasc Diabetol 2007; 6: 9.

    PubMed  Google Scholar 

  178. Lu L, Pu LJ, Zhang Q, Wang LJ, et al. Increased glycated albumin and decreased esRAGE levels are related to angiographic severity and extent of coronary artery disease in patients with type 2 diabetes. Atherosclerosis 2009; 206: 540–545.

    CAS  PubMed  Google Scholar 

  179. Yamagishi S, Adachi H, Nakamura K, Matsui T, et al. Positive association between serum levels of advanced glycation end products and the soluble form of receptor for advanced glycation end products in nondiabetic subjects. Metabolism 2006; 55: 1227–1231.

    CAS  PubMed  Google Scholar 

  180. Miura J, Yamamoto Y, Osawa M, Watanabe T, et al. Endogenous secretory receptor for advanced glycation endproducts levels are correlated with serum pentosidine and CML in patients with type 1 diabetes. Arterioscler Thromb Vasc Biol 2007; 27: 253–254.

    PubMed  Google Scholar 

  181. Koyama H, Shoji T, Fukumoto S, Shinohara K, et al. Low circulating endogenous secretory receptor for AGEs predicts cardiovascular mortality in patients with end-stage renal disease. Arterioscler Thromb Vasc Biol 2007; 27: 147–153.

    CAS  PubMed  Google Scholar 

  182. Geroldi D, Falcone C, Emanuele E, D’Angelo A, et al. Decreased plasma levels of soluble receptor for advanced glycation end-products in patients with essential hypertension. J Hypertens 2005; 23: 1725–1729.

    CAS  PubMed  Google Scholar 

  183. Basta G, Sironi AM, Lazzerini G, Del Turco S, et al. Circulating soluble receptor for advanced glycation end products is inversely associated with glycemic control and S100A12 protein. J Clin Endocrinol Metab 2006; 91: 4628–4634.

    CAS  PubMed  Google Scholar 

  184. Devangelio E, Santilli F, Formoso G, Ferroni P, et al. Soluble RAGE in type 2 diabetes: association with oxidative stress. Free Radic Biol Med 2007; 43: 511–518.

    CAS  PubMed  Google Scholar 

  185. Challier M, Jacqueminet S, Benabdesselam O, Grimaldi A, et al. Increased serum concentrations of soluble receptor for advanced glycation endproducts in patients with type 1 diabetes. Clin Chem 2005; 51: 1749–1750.

    CAS  PubMed  Google Scholar 

  186. Tan KC, Shiu SW, Chow WS, Leng L, et al. Association between serum levels of soluble receptor for advanced glycation end products and circulating advanced glycation end products in type 2 diabetes. Diabetologia 2006; 49: 2756–2762.

    CAS  PubMed  Google Scholar 

  187. Nakamura K, Yamagishi SI, Adachi H, Kurita-Nakamura Y, et al. Elevation of soluble form of receptor for advanced glycation end products (sRAGE) in diabetic subjects with coronary artery disease. Diabetes Metab Res Rev 2007; 23: 368–71.

    Google Scholar 

  188. Yamamoto Y, Miura J, Sakurai S, Watanabe T, et al. Assaying soluble forms of receptor for advanced glycation end products. Arterioscler Thromb Vasc Biol 2007; 27: e33–e34.

    CAS  Google Scholar 

  189. Humpert PM, Kopf S, Djuric Z, Wendt T, et al. Plasma sRAGE is independently associated with urinary albumin excretion in type 2 diabetes. Diabetes Care 2006; 29: 1111–1113.

    CAS  PubMed  Google Scholar 

  190. Kalousova M, Hodkova M, Kazderova M, Fialova J, et al. Soluble receptor for advanced glycation end products in patients with decreased renal function. Am J Kidney Dis 2006; 47: 406–411.

    CAS  PubMed  Google Scholar 

  191. Kalousova M, Bartosova K, Zima T, Skibova J, et al. Pregnancy-associated plasma protein a and soluble receptor for advanced glycation end products after kidney transplantation. Kidney Blood Press Res 2007; 30: 31–37.

    CAS  PubMed  Google Scholar 

  192. Gross S, van Ree RM, Oterdoom LH, de Vries AP, et al. Low levels of sRAGE are associated with increased risk for mortality in renal transplant recipients. Transplantation 2007; 84: 659–663.

    PubMed  Google Scholar 

  193. Kosaki A, Hasegawa T, Kimura T, Iida K, et al. Increased plasma S100A12 (EN-RAGE) levels in patients with type 2 diabetes. J Clin Endocrinol Metab 2004; 89: 5423–5428.

    CAS  PubMed  Google Scholar 

  194. Wendt TM, Tanji N, Guo J, Kislinger TR, et al. RAGE drives the development of glomerulosclerosis and implicates podocyte activation in the pathogenesis of diabetic nephropathy. Am J Pathol 2003; 162: 1123–1137.

    CAS  PubMed  Google Scholar 

  195. Arancio O, Zhang HP, Chen X, Lin C, et al. RAGE potentiates Abeta-induced perturbation of neuronal function in transgenic mice. Embo J 2004; 23: 4096–4105.

    CAS  PubMed  Google Scholar 

  196. Cheng C, Tsuneyama K, Kominami R, Shinohara H, et al. Expression profiling of endogenous secretory receptor for advanced glycation end products in human organs. Mod Pathol 2005; 18: 1385–1396.

    CAS  PubMed  Google Scholar 

  197. Tanaka N, Yonekura H, Yamagishi S, Fujimori H, et al. The receptor for advanced glycation end products is induced by the glycation products themselves and tumor necrosis factor-alpha through nuclear factor-kappa B, and by 17beta-estradiol through Sp-1 in human vascular endothelial cells. J Biol Chem 2000; 275: 25781–25790.

    CAS  PubMed  Google Scholar 

  198. Coughlan MT, Thallas-Bonke V, Pete J, Long DM, et al. Combination therapy with the advanced glycation end product cross-link breaker, alagebrium, and angiotensin converting enzyme inhibitors in diabetes: synergy or redundancy? Endocrinology 2007; 148: 886–895.

    CAS  PubMed  Google Scholar 

  199. Zhong Y, Li SH, Liu SM, Szmitko PE, et al. C-Reactive protein upregulates receptor for advanced glycation end products expression in human endothelial cells. Hypertension 2006; 48: 504–511.

    CAS  PubMed  Google Scholar 

  200. Geroldi D, Falcone C, Minoretti P, Emanuele E, et al. High levels of soluble receptor for advanced glycation end products may be a marker of extreme longevity in humans. J Am Geriatr Soc 2006; 54: 1149–1150.

    PubMed  Google Scholar 

  201. Forbes JM, Thorpe SR, Thallas-Bonke V, Pete J, et al. Modulation of soluble receptor for advanced glycation end products by angiotensin-converting enzyme-1 inhibition in diabetic nephropathy. J Am Soc Nephrol 2005; 16: 2363–2372.

    CAS  PubMed  Google Scholar 

  202. Marx N, Walcher D, Ivanova N, Rautzenberg K, et al. Thiazolidinediones reduce endothelial expression of receptors for advanced glycation end products. Diabetes 2004; 53: 2662–2668.

    CAS  PubMed  Google Scholar 

  203. Okamoto T, Yamagishi S, Inagaki Y, Amano S, et al. Angiogenesis induced by advanced glycation end products and its prevention by cerivastatin. Faseb J 2002; 16: 1928–1930.

    CAS  PubMed  Google Scholar 

  204. Cuccurullo C, Iezzi A, Fazia ML, De Cesare D, et al. Suppression of RAGE as a basis of simvastatin-dependent plaque stabilization in type 2 diabetes. Arterioscler Thromb Vasc Biol 2006; 26: 2716–2723.

    CAS  PubMed  Google Scholar 

  205. Tan KC, Chow WS, Tso AW, Xu A, et al. Thiazolidinedione increases serum soluble receptor for advanced glycation end-products in type 2 diabetes. Diabetologia 2007; 50: 1819–1825.

    CAS  PubMed  Google Scholar 

  206. Tam HL, Shiu SW, Wong Y, Chow WS, et al. Effects of atorvastatin on serum soluble receptors for advanced glycation end-products in type 2 diabetes. Atherosclerosis 2010; 209: 173–177.

    CAS  PubMed  Google Scholar 

  207. Takeuchi M, Yanase Y, Matsuura N, Yamagishi Si S, et al. Immunological detection of a novel advanced glycation end-product. Mol Med 2001; 7: 783–791.

    CAS  Google Scholar 

  208. Katakami N, Matsuhisa M, Kaneto H, Matsuoka TA, et al. Serum endogenous secretory RAGE level is an independent risk factor for the progression of carotid atherosclerosis in type 1 diabetes. Atherosclerosis 2009; 204: 288–292.

    CAS  PubMed  Google Scholar 

  209. Koyama Y, Takeishi Y, Niizeki T, Suzuki S, et al. Soluble Receptor for advanced glycation end products (RAGE) is a prognostic factor for heart failure. J Card Fail 2008; 14: 133–139.

    CAS  PubMed  Google Scholar 

  210. Kalousova M, Jachymova M, Mestek O, Hodkova M, et al. Receptor for advanced glycation end products – soluble form and gene polymorphisms in chronic haemodialysis patients. Nephrol Dial Transplant 2007; 22: 2020–2026.

    CAS  PubMed  Google Scholar 

  211. Nakamura K, Yamagishi S, Adachi H, Kurita-Nakamura Y, et al. Serum levels of sRAGE, the soluble form of receptor for advanced glycation end products, are associated with inflammatory markers in patients with type 2 diabetes. Mol Med 2007; 13: 185–189.

    CAS  PubMed  Google Scholar 

  212. Nakamura K, Yamagishi SI, Adachi H, Matsui T, et al. Circulating advanced glycation end products (AGEs) and soluble form of receptor for AGEs (sRAGE) are independent determinants of serum monocyte chemoattractant protein-1 (MCP-1) levels in patients with type 2 diabetes. Diabetes Metab Res Rev 2008; 24: 109–114.

    CAS  PubMed  Google Scholar 

  213. Nakamura K, Yamagishi S, Adachi H, Matsui T, et al. Serum levels of soluble form of receptor for advanced glycation end products (sRAGE) are positively associated with circulating AGEs and soluble form of VCAM-1 in patients with type 2 diabetes. Microvasc Res 2008; 76: 52–56.

    CAS  PubMed  Google Scholar 

  214. Choi KM, Yoo HJ, Kim HY, Lee KW, et al. Association between endogenous secretory RAGE, inflammatory markers and arterial stiffness. Int J Cardiol 2009; 132: 96–101.

    CAS  PubMed  Google Scholar 

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Acknowledgments

We thank our colleagues in the Osaka City University Graduate School of Medicine and Kanazawa University Graduate School of Medical Science for their unflagging support of our projects. We apologize to all colleagues whose work we could not cite other than indirectly through other publications, due to limitation of space. This study was supported in part by a Grant-in-Aid for Scientific Research (20591067 to HK) from the Ministry of Education, Culture, Sports, Science and Technology, Japan.

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  1. Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University School of Medicine, 1-4-3, Asahi-machi, Abeno, Osaka, 545-8585, Japan

    Hidenori Koyama

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  1. Hidenori Koyama
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  2. Yoshiki Nishizawa
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Correspondence to Hidenori Koyama .

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  1. Graduate School of Medicine, Division of Molecular Medicine and Thera, Tohoku University, Seiryo-machi 2-1, Sendai, 980-8575, Japan

    Toshio Miyata

  2. Medizinische Klinik IV, Universitätsklinikum Erlangen, Krankenhausstr. 12, Erlangen, 91054, Germany

    Kai-Uwe Eckardt

  3. Graduate School of Medicine &, Faculty of Medicine, University of Tokyo, Hongo 7-3-1, Tokyo, 113-8655, Japan

    Masaomi Nangaku

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Koyama, H., Nishizawa, Y. (2011). Cardiovascular Complications in Renal Failure: Implications of Advanced Glycation End Products and Their Receptor RAGE. In: Miyata, T., Eckardt, KU., Nangaku, M. (eds) Studies on Renal Disorders. Oxidative Stress in Applied Basic Research and Clinical Practice. Humana Press. https://doi.org/10.1007/978-1-60761-857-7_13

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