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Relationship of Advanced Glycation End Products With Cardiovascular Disease in Menopausal Women

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Abstract

Cardiovascular disease (CVD) represents the most significant cause of death in postmenopausal women. Advanced glycation end products (AGEs) are formed by nonenzymatic modification of proteins, lipids, and nucleic acids by glucose. This review focuses on the contribution of AGEs and their receptors to the development of CVD in menopause. Advanced glycation end products circulate and activate the proinflammatory endothelial cell surface receptor called RAGE, bind to the extracellular matrix of the cardiovascular system, or bind to the circulating anti-inflammatory soluble form of RAGE (sRAGE). Data emerging from human and animal studies suggest that AGEs and both receptors (RAGE and sRAGE) are implicated in the pathophysiology of CVD. Particular emphasis has been given to the role of AGE–RAGE axis in oxidative stress, inflammation, endothelial cell toxicity, and progression of atherosclerosis in menopause. Data accruing from human and animal studies suggest that RAGE expression level and circulating sRAGE level are associated with estradiol and are correlated with CVD risk factors, such as adiposity, dyslipidemia, insulin resistance, diabetes, and metabolic syndrome. By recognizing the impact of AGEs on atherosclerosis, pharmacological strategies targeting the AGE–RAGE pathway hold therapeutic potential for CVD in menopausal women.

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References

  1. Roger VL, Go AS, Lloyd-Jones DM, et al. American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2012 update: a report from the American Heart Association. Circulation. 2012; 125(22): e2–e220.

    PubMed  Google Scholar 

  2. Piperi C, Adamopoulos C, Dalagiorgou G, Diamanti-Kandarakis E, Papavassiliou AG. Crosstalk between advanced glycation and endoplasmic reticulum stress: emerging therapeutic targeting for metabolic diseases. J Clin Endocrinol Metab. 2012;97(7): 2231–2242.

    CAS  PubMed  Google Scholar 

  3. Falcone C, Bozzini S, Guasti L, et al. Soluble RAGE plasma levels in patients with coronary artery disease and peripheral artery disease. Scientific World Journal. 2013;2013:584–504.

    Google Scholar 

  4. Chiang KH, Huang PH, Huang SS, Wu TC, Chen JW, Lin SJ. Plasma levels of soluble receptor for advanced glycation end products are associated with endothelial function and predict cardiovascular events in nondiabetic patients. Coron Artery Dis. 2009;20(4):267–273.

    PubMed  Google Scholar 

  5. Bodiga VL, Eda SR, Bodiga S. Advanced glycation end products: role in pathology of diabetic cardiomyopathy. Heart Fail Rev. 2013;19(1):49–63.

    Google Scholar 

  6. Yan SF, Ramasamy R, Schmidt AM. Receptor for AGE (RAGE) and its ligands-cast into leading roles in diabetes and the inflammatory response. J Mol Med (Berl). 2009;87(3):235–247.

    CAS  PubMed  PubMed Central  Google Scholar 

  7. Uribarri J, Woodruff S, Goodman S, et al. Advanced glycation end products in foods and a practical guide to their reduction in the diet. J Am Diet Assoc. 2010; 110(6):911–16.e12.

    PubMed  PubMed Central  Google Scholar 

  8. Uribarri J, Cai W, Peppa M, et al. Circulating glycotoxins and dietary advanced glycation endproducts: two links to inflammatory response, oxidative stress, and aging. J Gerontol A Biol Sci Med Sci. 2007;62(4):427–433.

    PubMed  PubMed Central  Google Scholar 

  9. Goldberg T, Cai W, Peppa M, et al. Advanced glycoxidation end products in commonly consumed foods. J Am Diet Assoc. 2004; 104(8):1287–1291.

    CAS  PubMed  Google Scholar 

  10. Vlassara H, Cai W, Crandall J, et al. Inflammatory mediators are induced by dietary glycotoxins, a major risk factor for diabetic angiopathy. Proc Natl Acad Sci USA. 2002;99(24): 15596–15601.

    CAS  PubMed  Google Scholar 

  11. Vlassara H, Cai W, Goodman S, et al. Protection against loss of innate defenses in adulthood by low advanced glycation end products (AGE) intake: role of the antiinflammatory AGE receptor-1. J Clin Endocrinol Metab. 2009;94(11):4483–4491.

    CAS  PubMed  PubMed Central  Google Scholar 

  12. Schmidt AM, Vianna M, Gerlach M, 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(21):14987–14997.

    CAS  PubMed  Google Scholar 

  13. Sugaya K, Fukagawa T, Matsumoto K, et al. Three genes in the human MHC class III region near the junction with the class II gene for receptor of advanced glycosylation end products, PBX2 homeobox gene and a notch homolog, human counterpart of mouse mammary tumor gene int-3. Genomics. 1994; 23(2):408–419.

    CAS  PubMed  Google Scholar 

  14. Schmidt AM, Hori O, Chen JX, 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(3):1395–1403.

    CAS  PubMed  PubMed Central  Google Scholar 

  15. Giacco F, Brownlee M. Oxidative stress and diabetic complications. Circ Res. 2010;107(9):1058–10570.

    CAS  PubMed  PubMed Central  Google Scholar 

  16. Ramasamy R, Yan SF, Schmidt AM. Advanced glycation endproducts: from precursors to RAGE: round and round we go. Amino Acids. 2012;42(4):1151–11561.

    CAS  PubMed  Google Scholar 

  17. Kuzan A, Chwiłkowska A, Kobielarz M, Pezowicz C, Gamian A. Glycation of extracellular matrix proteins and its role in atherosclerosis [in Polish]. Postepy Hig Med Dosw (Online). 2012;66: 804–809.

    PubMed  Google Scholar 

  18. Ramasamy R, Schmidt AM. Receptor for advanced glycation end products (RAGE) and implications for the pathophysiology of heart failure. Curr Heart Fail Rep. 2012;9(2):107–116.

    CAS  PubMed  PubMed Central  Google Scholar 

  19. Schmidt AM, Hasu M, Popov D, et al. Receptor for advanced glycation end products (AGEs) has a central role in vessel wall interactions and gene activation in response to circulating AGE proteins. Proc Natl Acad Sci USA. 1994;91(19):8807–8811.

    CAS  PubMed  Google Scholar 

  20. Schmidt AM, Stern DM. Receptor for age (RAGE) is a gene within the major histocompatibility class III region: implications for host response mechanisms in homeostasis and chronic disease. Front Biosci. 2001;6:D1151–D1160.

    CAS  PubMed  Google Scholar 

  21. Mahajan N, Malik N, Bahl A, Dhawan V. Receptor for advanced glycation end products (RAGE) and its inflammatory ligand EN-RAGE in non-diabetic subjects with pre-mature coronary artery disease. Atherosclerosis. 2009;207(2):597–602.

    CAS  PubMed  Google Scholar 

  22. Fujisawa K, Katakami N, Kaneto H, et al. Circulating soluble RAGE as a predictive biomarker of cardiovascular event risk in patients with type 2 diabetes. Atherosclerosis. 2013;227(2):425–428.

    CAS  PubMed  Google Scholar 

  23. Selvin E, Halushka MK, Rawlings AM, et al. sRAGE and risk of diabetes, cardiovascular disease, and death. Diabetes. 2013;62(6): 2116–2121.

    CAS  PubMed  PubMed Central  Google Scholar 

  24. Falcone C, Emanuele E, D’Angelo A, 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(5):1032–1037.

    CAS  PubMed  Google Scholar 

  25. Falcone C, Buzzi MP, Bozzini S, et al; TALENT Investigators. Relationship between sRAGE and eotaxin-3 with CRP in hypertensive patients at high cardiovascular risk. J Nephrol. 2013; 26(1):144–151.

    CAS  PubMed  Google Scholar 

  26. Geroldi D, Falcone C, Emanuele E, et al. Decreased plasma levels of soluble receptor for advanced glycation end-products in patients with essential hypertension. J Hypertension. 2005;23(9):1725–1729.

    CAS  Google Scholar 

  27. Frommhold D, Kamphues A, Hepper I, et al. RAGE and ICAM-1 cooperate in mediating leukocyte recruitment during acute inflammation in vivo. Blood. 2010;116(5):841–849.

    CAS  PubMed  Google Scholar 

  28. Ha CH, Kim S, Chung J, et al. Inhibitory effect of soluble RAGE in disturbed flow-induced atherogenesis. Int J Mol Med. 2013; 32(2):373–380.

    CAS  PubMed  Google Scholar 

  29. Choi KM, Han KA, Ahn HJ, et al. Effects of exercise on sRAGE levels and cardiometabolic risk factors in patients with type 2 diabetes: a randomized controlled trial. J Clin Endocrinol Metab. 2012;97(10):3751–3758.

    CAS  PubMed  Google Scholar 

  30. Semba RD, Ferrucci L, Sun K, et al. Advanced glycation end products and their circulating receptors predict cardiovascular disease mortality in older community-dwelling women. Aging Clin Exp Res. 2009;2(2):182–190.

    Google Scholar 

  31. Pulkkinen A, Viitanen L, Kareinen A, Lehto S, Laakso M. Gly82-Ser polymorphism of the receptor of advanced glycation end product gene is not associated with coronary heart disease in Finnish nondiabetic subjects or in patients with type 2 diabetes. Diabetes Care. 2000; 23(6):864.

    CAS  PubMed  Google Scholar 

  32. Hudson BI, Stickland MH, Grant PJ. Identification of polymorphisms in the receptor for advanced glycation end products (RAGE) gene: prevalence in type 2 diabetes and ethnic groups. Diabetes. 1998;47(7):1155–1157.

    CAS  PubMed  Google Scholar 

  33. Hofmann MA, Yang Q, Harja E, et al. The RAGE Gly82Ser polymorphism is not associated with cardiovascular disease in the Framingham offspring study. Atherosclerosis. 2005;182(2):301–305.

    CAS  PubMed  Google Scholar 

  34. Bansal S, Chawla D, Banerjee BD, Madhu SV, Tripathi AK. Association of RAGE gene polymorphism with circulating AGEs level and paraoxonase activity in relation to macro-vascular complications in Indian type 2 diabetes mellitus(T2DM) patients. Gene. 2013;526(2):325–330.

    CAS  PubMed  Google Scholar 

  35. Koyama H, Shoji T, Yokoyama H, et al. Plasma level of endogenous secretory RAGE is associated with components of the metabolic syndrome and atherosclerosis. Arterioscler Thromb Vasc Biol. 2005;25(12):2587–2593.

    CAS  PubMed  Google Scholar 

  36. Sebeková K, Krivošíková Z, Gajdoš M. Total plasma Nɛ-(carbox-ymethyl)lysine and sRAGE levels are inversely associated with a number of metabolic syndrome risk factors in non-diabetic young-to-middle-aged medication-free subjects. Clin Chem Lab Med. 2014;52(1):139–149.

    PubMed  Google Scholar 

  37. Norata GD, Garlaschelli K, Grigore L, et al. Circulating soluble receptor for advanced glycation end products is inversely associated with body mass index and waist/hip ratio in the general population. Nutr Metab Cardiovasc Dis. 2009;19(2):129–134.

    CAS  PubMed  Google Scholar 

  38. Kaur J. A comprehensive review on metabolic syndrome. Cardiol Res Pract. 2014;2014:943162.

    PubMed  PubMed Central  Google Scholar 

  39. Petersen KF, Shulman GI. Etiology of insulin resistance. Am J Med. 2006;119(5 suppl 1):S10–S16.

    PubMed  PubMed Central  Google Scholar 

  40. Lindheim SR, Presser SC, Ditkoff EC, Vijod MA, Stanczyk FZ, Lobo RA. A possible bimodal effect of estrogen on insulin sensitivity in postmenopausal women and the attenuating effect of added progestin. Fertil Steril. 1993;60(4):664–667.

    CAS  PubMed  Google Scholar 

  41. Lindheim SR, Buchanan TA, Duffy DM, et al. Comparison of estimates of insulin sensitivity in pre- and postmenopausal women using the insulin tolerance test and the frequently sampled intravenous glucose tolerance test. J Soc Gynecol Investig. 1994; 1(2):150–154.

    CAS  PubMed  Google Scholar 

  42. Unoki H, Yamagishi S. Advanced glycation end products and insulin resistance. Curr Pharm Des. 2008;14(10):987–989.

    CAS  PubMed  Google Scholar 

  43. Sullivan CM, Futers TS, Barrett JH, Hudson BI, Freeman MS, Grant PJ. RAGE polymorphisms and the heritability of insulin resistance: the Leeds family study. Diab Vase Dis Res. 2005; 2(1):42–44.

    Google Scholar 

  44. Tan KC, Shiu SW, Wong Y, Tarn X. Serum advanced glycation end products (AGEs) are associated with insulin resistance. Diabetes Metab Res Rev. 2011;27(5):488–492.

    CAS  PubMed  Google Scholar 

  45. Miele C, Riboulet A, Maitan MA, et al. Human glycated albumin affects glucose metabolism in L6 skeletal muscle cells by impairing insulin-induced insulin receptor substrate (IRS) signaling through a protein kinase C alpha-mediated mechanism. J Biol Chem. 2003;278(48):47376–47387.

    CAS  PubMed  Google Scholar 

  46. Jia X, Wu L. Accumulation of endogenous methylglyoxal impaired insulin signaling in adipose tissue of fructose-fed rats. Mol Cell Biochem. 2007;306(1–2):133–139.

    CAS  PubMed  Google Scholar 

  47. Cai W, Ramdas M, Zhu L, Chen X, Striker GE, Vlassara H. Oral advanced glycation endproducts (AGEs) promote insulin resistance and diabetes by depleting the antioxidant defenses AGE receptor-1 and sirtuin 1. Proc Natl Acad Sci USA. 2012;109(39):15888–15893.

    CAS  PubMed  Google Scholar 

  48. Uchida Y, Ohba K, Yoshioka T, Irie K, Muraki T, Maru Y. Cellular carbonyl stress enhances the expression of plasminogen activator inhibitor-1 in rat white adipocytes via reactive oxygen species-dependent pathway. J Biol Chem. 2004; 279(6):4075–4083.

    CAS  PubMed  Google Scholar 

  49. Fan X, Subramaniam R, Weiss MF, Monnier VM. Methylglyoxal-bovine serum albumin stimulates tumor necrosis factor alpha secretion in RAW 264.7 cells through activation of mitogen-activating protein kinase, nuclear factor kappaB and intracellular reactive oxygen species formation. Arch Biochem Biophys. 2003; 409(2):274–286.

    CAS  PubMed  Google Scholar 

  50. Matthews KA, Crawford SL, Chae CU, et al. Are changes in cardiovascular disease risk factors in midlife women due to chronological aging or to the menopausal transition? J Am Coll Cardiol. 2009;54(25):2366–2373.

    CAS  PubMed  PubMed Central  Google Scholar 

  51. Berg G, Mesch V, Boero L, et al. Lipid and lipoprotein profile in menopausal transition. Effects of hormones, age and fat distribution. Horm Metab Res. 2004;36(4):215–220.

    CAS  PubMed  Google Scholar 

  52. Derby CA, Crawford SL, Pasternak RC, Sowers M, Sternfeld B, Matthews KA. Lipid changes during the menopause transition in relation to age and weight: the Study of Women’s Health Across the Nation. Am J Epidemiol. 2009;169(11):1352–1361.

    PubMed  PubMed Central  Google Scholar 

  53. Matthews KA, Meilahn E, Kuiler LH, Kelsey SF, Caggiula AW, Wing RR. Menopause and risk factors for coronary heart disease. N Engl J Med. 1989;321(10):641–646.

    CAS  PubMed  Google Scholar 

  54. Fan AZ, Dwyer JH. Sex differences in the relation of HDL cholesterol to progression of carotid intima-media thickness: the Los Angeles Atherosclerosis Study. Atherosclerosis. 2007; 195(1): e191–e196.

    CAS  PubMed  Google Scholar 

  55. Woodard GA, Brooks MM, Barinas-Mitchell E, Mackey RH, Matthews KA, Sutton-Tyrrell K. Lipids, menopause, and early atherosclerosis in Study of Women’s Health Across the Nation Heart women. Menopause. 2011;18(4):376–384.

    PubMed  PubMed Central  Google Scholar 

  56. Lopes-Virella MF, Hunt KJ, Baker NL, et al. Levels of oxidized LDL and advanced glycation end products-modified LDL in circulating immune complexes are strongly associated with increased levels of carotid intima-media thickness and its progression in type 1 diabetes. Diabetes. 2011;60(2):582–589.

    CAS  PubMed  PubMed Central  Google Scholar 

  57. Hunt KJ, Baker N, Cleary P, et al; DCCT/EDIC Research Group. Oxidized LDL and AGE-LDL in circulating immune complexes strongly predict progression of carotid artery IMT in type 1 diabetes. Atherosclerosis. 2013;231(2):315–322.

    CAS  PubMed  PubMed Central  Google Scholar 

  58. Turk Z, Cavlovic-Naglic M, Turk N. Relationship of methylglyoxal-adduct biogenesis to LDL and triglyceride levels in diabetics. Life Sci. 2011;89(13–14):485–490.

    CAS  PubMed  Google Scholar 

  59. Jinnouchi Y, Yamagishi S, Takeuchi M, et al. Atorvastatin decreases serum levels of advanced glycation end products (AGEs) in patients with type 2 diabetes. Clin Exp Med. 2006;6(4): 191–193.

    CAS  PubMed  Google Scholar 

  60. Quade-Lyssy P, Kanarek AM, Baiersdörfer M, Postina R, Kojro E. Statins stimulate the production of a soluble form of the receptor for advanced glycation end products. J Lipid Res. 2013;54(11): 3052–3061.

    CAS  PubMed  PubMed Central  Google Scholar 

  61. Lu L, Peng WH, Wang W, Wang LJ, Chen QJ, Shen WF. Effects of atorvastatin on progression of diabetic nephropathy and local RAGE and soluble RAGE expressions in rats. J Zhejiang Univ Sci B. 2011;12(8):652–659.

    CAS  PubMed  PubMed Central  Google Scholar 

  62. Santilli F, Bucciarelli L, Noto D, et al. Decreased plasma soluble RAGE in patients with hypercholesterolemia: effects of statins. Free Radic Biol Med. 2007;43(9):1255–1262.

    CAS  PubMed  Google Scholar 

  63. Tarn HL, Shiu SW, Wong Y, Chow WS, Betteridge DJ, Tan KC. Effects of atorvastatin on serum soluble receptors for advanced glycation end-products in type 2 diabetes. Atherosclerosis. 2010;209(1):173–177.

    Google Scholar 

  64. Colhoun HM, Betteridge DJ, Durrington P, et al. Total soluble and endogenous secretory receptor for advanced glycation end products as predictive biomarkers of coronary heart disease risk in patients with type 2 diabetes: an analysis from the CARDS trial. Diabetes. 2011;60(9):2379–2385.

    CAS  PubMed  PubMed Central  Google Scholar 

  65. Mukhopadhyay S, Mukherjee TK. Bridging advanced glycation end product, receptor for advanced glycation end product and nitric oxide with hormonal replacement/estrogen therapy in healthy versus diabetic postmenopausal women: a perspective. Biochim Biophys Acta. 2005;1745(2):145–155.

    CAS  PubMed  Google Scholar 

  66. Merhi Z. Advanced glycation end-products: pathway of potentially significant pathophysiological and therapeutic relevance for metabolic syndrome in menopausal women. J Clin Endocrinol Metab. 2014;99(4): 1146–1148.

    CAS  PubMed  Google Scholar 

  67. Tanaka N, Yonekura H, Yamagishi S, Fujimori H, Yamamoto Y, Yamamoto H. The receptor for advanced glycosylation end products is induced by the glycation product themselves and TNF-alpha through nuclear factor kappa B and by 17-beta-estradiol through Spl in human vascular endothelial cells. J Biol Chem. 2000;275(33):25781–25790.

    CAS  PubMed  Google Scholar 

  68. Mukherjee TK, Nathan L, Dinh H, Reddy ST, Chaudhuri G. 17-epiestriol, an estrogen metabolite, is more potent than estradiol in inhibiting vascular cell adhesion molecule 1 (VCAM1) mRNA expression. J Biol Chem. 2003;278(14):11746–11752.

    CAS  PubMed  Google Scholar 

  69. Pullerits R, d’Elia HF, Tarkowski A, Carlsten H. The decrease of soluble RAGE levels in rheumatoid arthritis patients following hormone replacement therapy is associated with increased bone mineral density and diminished bone/cartilage turnover: a randomized controlled trial. Rheumatology (Oxford). 2009;48(7):785–790.

    CAS  PubMed  Google Scholar 

  70. Merhi Z. Advanced glycation end products and their relevance in female reproduction. Hum Reprod. 2014;29(1):135–145.

    CAS  PubMed  Google Scholar 

  71. Bucala R, Makita Z, Vega G, 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 USA. 1994;91(20):9441–9445.

    CAS  PubMed  Google Scholar 

  72. Hu C, Cong XD, Dai DZ, Zhang Y, Zhang GL, Dai Y. Argirein alleviates diabetic nephropathy through attenuating NADPH oxidase, Cx43, and PERK in renal tissue. Naunyn Schmiedebergs Arch Pharmacol. 2011;383(3):309–319.

    CAS  PubMed  Google Scholar 

  73. Adisakwattana S, Sompong W, Meeprom A, Ngamukote S, Yibchok-Anun S. Cinnamic acid and its derivatives inhibit fructose-mediated protein glycation. Lnt J Mol Sci. 2012;13(2): 1778–1789.

    CAS  Google Scholar 

  74. Meeprom A, Sompong W, Chan CB, Adisakwattana S. Isoferulic acid, a new anti-glycation agent, inhibits fructose- and glucose-mediated protein glycation in vitro. Molecules. 2013;18(6): 6439–6454.

    CAS  PubMed  PubMed Central  Google Scholar 

  75. Chang KC, Liang JT, Tsai PS, Wu MS, Hsu KL. Prevention of arterial stiffening by pyridoxamine in diabetes is associated with inhibition of the pathogenic glycation on aortic collagen. Br J Pharmacol. 2009;157(8):1419–1426.

    CAS  PubMed  PubMed Central  Google Scholar 

  76. Degenhardt TP, Alderson NL, Arrington DD, et al. Pyridoxamine inhibits early renal disease and dyslipidemia in the streptozotocin-diabetic rat. Kidney Lnt. 2000;61(3):939–950.

    Google Scholar 

  77. Williams ME, Bolton WK, Khalifah RG, Degenhardt TP, Schot-zinger RJ, McGill JB. Effects of pyridoxamine in combined phase 2 studies of patients with type 1 and type 2 diabetes and overt nephropathy. Am J Nephrol. 2007;27(6):605–614.

    CAS  PubMed  Google Scholar 

  78. Shepler B, Nash C, Smith C, Dimarco A, Petty J, Szewciw S. Update on potential drugs for the treatment of diabetic kidney disease. Clin Ther. 2012;34(6):1237–1246.

    CAS  PubMed  Google Scholar 

  79. Usta MF, Kendirci M, Gur S, et al. The breakdown of preformed advanced glycation end products reverses erectile dysfunction in streptozotocin-induced diabetic rats: preventive versus curative treatment. J Sex Med. 2006;3(2):242–250.

    CAS  PubMed  Google Scholar 

  80. Kass DA, Shapiro EP, Kawaguchi M, et al. Improved arterial compliance by a novel advanced glycation end-product crosslink breaker. Circulation. 2001;104(13):1464–1470.

    CAS  PubMed  Google Scholar 

  81. Zieman SJ, Melenovsky V, Clattenburg L, et al. Advanced glycation endproduct crosslink breaker (alagebrium) improves endothelial function in patients with isolated systolic hypertension. J Hypertens. 2007;25(3):577–583.

    CAS  PubMed  Google Scholar 

  82. Nagai R, Murray DB, Metz TO, Baynes JW. Chelation: a fundamental mechanism of action of AGE inhibitors, AGE breakers, and other inhibitors of diabetes complications. Diabetes. 2012;61(3):549–559.

    CAS  PubMed  PubMed Central  Google Scholar 

  83. Cooper GJ. Selective divalent copper chelation for the treatment of diabetes mellitus. Curr Med Chem. 2012;19(17):2828–2860.

    CAS  PubMed  Google Scholar 

  84. Frizzell N, Baynes JW. Chelation therapy for the management of diabetic complications: a hypothesis and a proposal for clinical laboratory assessment of metal ion homeostasis in plasma. Clin Chem Lab Med. 2014;52:69–75.

    CAS  PubMed  Google Scholar 

  85. Ahmad S, Shahab U, Baig MH, et al. Inhibitory effect of metformin and pyridoxamine in the formation of early, intermediate and advanced glycation end-products. PLoS One. 2013; 8(9): e72128.

    CAS  PubMed  PubMed Central  Google Scholar 

  86. Yamagishi S, Amano S, Inagaki Y, Okamoto T, Takeuchi M, Makita Z. Beraprost sodium, a prostaglandin 12 analogue, protects against advanced glycation end products-induced injury in cultured retinal pericytes. Mol Med. 2002;8(9):546–550.

    CAS  PubMed  PubMed Central  Google Scholar 

  87. Meerwaldt R, van der Vaart MG, van Dam GM, et al. Clinical relevance of advanced glycation endproducts for vascular surgery. Eur J Vasc Endovasc Surg. 2008;36(2):125–131.

    CAS  PubMed  Google Scholar 

  88. Jariyapamornkoon N, Yibchok-anun S, Adisakwattana S. Inhibition of advanced glycation end products by red grape skin extract and its antioxidant activity. BMC Complement Altern Med. 2013; 13:171–191.

    PubMed  PubMed Central  Google Scholar 

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Pertynska-Marczewska, M., Merhi, Z. Relationship of Advanced Glycation End Products With Cardiovascular Disease in Menopausal Women. Reprod. Sci. 22, 774–782 (2015). https://doi.org/10.1177/1933719114549845

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