Skip to main content
Erschienen in: Current Diabetes Reports 4/2011

01.08.2011

AGEs, RAGE, and Diabetic Retinopathy

verfasst von: Hongliang Zong, Micheal Ward, Alan W. Stitt

Erschienen in: Current Diabetes Reports | Ausgabe 4/2011

Einloggen, um Zugang zu erhalten

Abstract

Diabetic retinopathy is a major diabetic complication with a highly complex etiology. Although there are many pathways involved, it has become established that chronic exposure of the retina to hyperglycemia gives rise to accumulation of advanced glycation end products (AGEs) that play an important role in retinopathy. In addition, the receptor for AGEs (RAGE) is ubiquitously expressed in various retinal cells and is upregulated in the retinas of diabetic patients, resulting in activation of pro-oxidant and proinflammatory signaling pathways. This AGE-RAGE axis appears to play a central role in the sustained inflammation, neurodegeneration, and retinal microvascular dysfunction occurring during diabetic retinopathy. The nature of AGE formation and RAGE signaling bring forward possibilities for therapeutic intervention. The multiple components of the AGE-RAGE axis, including signal transduction, formation of ligands, and the end-point effectors, may be promising targets for strategies to treat diabetic retinopathy.
Literatur
1.
2.
Zurück zum Zitat Zhang X, Saaddine JB, Chou CF, et al. Prevalence of diabetic retinopathy in the United States, 2005–2008. JAMA. 2010;304:649–56.PubMedCrossRef Zhang X, Saaddine JB, Chou CF, et al. Prevalence of diabetic retinopathy in the United States, 2005–2008. JAMA. 2010;304:649–56.PubMedCrossRef
3.
Zurück zum Zitat Mohamed Q, Gillies MC, Wong TY. Management of diabetic retinopathy: a systematic review. JAMA. 2007;298:902–16.PubMedCrossRef Mohamed Q, Gillies MC, Wong TY. Management of diabetic retinopathy: a systematic review. JAMA. 2007;298:902–16.PubMedCrossRef
4.
Zurück zum Zitat Mannervik B. Molecular enzymology of the glyoxalase system. Drug Metabol Drug Interact. 2008;23:13–27.PubMedCrossRef Mannervik B. Molecular enzymology of the glyoxalase system. Drug Metabol Drug Interact. 2008;23:13–27.PubMedCrossRef
5.
Zurück zum Zitat Goldberg T, Cai W, Peppa M, et al. Advanced glycoxidation end products in commonly consumed foods. J Am Diet Assoc. 2004;104:1287–91.PubMedCrossRef Goldberg T, Cai W, Peppa M, et al. Advanced glycoxidation end products in commonly consumed foods. J Am Diet Assoc. 2004;104:1287–91.PubMedCrossRef
6.
Zurück zum Zitat Chao PC, Huang CN, Hsu CC, Yin MC, Guo YR. Association of dietary AGEs with circulating AGEs, glycated LDL, IL-1alpha and MCP-1 levels in type 2 diabetic patients. Eur J Nutr. 2010;49:429–34.PubMedCrossRef Chao PC, Huang CN, Hsu CC, Yin MC, Guo YR. Association of dietary AGEs with circulating AGEs, glycated LDL, IL-1alpha and MCP-1 levels in type 2 diabetic patients. Eur J Nutr. 2010;49:429–34.PubMedCrossRef
7.
Zurück zum Zitat Cai W, Gao QD, Zhu L, Peppa M, He C, Vlassara H. Oxidative stress-inducing carbonyl compounds from common foods: novel mediators of cellular dysfunction. Mol Med. 2002;8:337–46.PubMed Cai W, Gao QD, Zhu L, Peppa M, He C, Vlassara H. Oxidative stress-inducing carbonyl compounds from common foods: novel mediators of cellular dysfunction. Mol Med. 2002;8:337–46.PubMed
8.
Zurück zum Zitat Uribarri J, Cai W, Sandu O, Peppa M, Goldberg T, Vlassara H. Diet-derived advanced glycation end products are major contributors to the body’s AGE pool and induce inflammation in healthy subjects. Ann NY Acad Sci. 2005;1043:461–6.PubMedCrossRef Uribarri J, Cai W, Sandu O, Peppa M, Goldberg T, Vlassara H. Diet-derived advanced glycation end products are major contributors to the body’s AGE pool and induce inflammation in healthy subjects. Ann NY Acad Sci. 2005;1043:461–6.PubMedCrossRef
9.
Zurück zum Zitat Goh SY, Cooper ME. Clinical review: the role of advanced glycation end products in progression and complications of diabetes. J Clin Endocrinol Metab. 2008;93:1143–52.PubMedCrossRef Goh SY, Cooper ME. Clinical review: the role of advanced glycation end products in progression and complications of diabetes. J Clin Endocrinol Metab. 2008;93:1143–52.PubMedCrossRef
10.
Zurück zum Zitat Vlassara H. The AGE-receptor in the pathogenesis of diabetic complications. Diab Metab Res Rev. 2001;17:436–43.CrossRef Vlassara H. The AGE-receptor in the pathogenesis of diabetic complications. Diab Metab Res Rev. 2001;17:436–43.CrossRef
11.
Zurück zum Zitat 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;267:14987–97.PubMed 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;267:14987–97.PubMed
12.
Zurück zum Zitat • Kalea AZ, Schmidt AM, Hudson BI. RAGE: a novel biological and genetic marker for vascular disease. Clin Sci (Lond) 2009, 116:621–637. This study has had an important impact because it reviewed the role of RAGE in the pathogenesis of vascular disease and contains all the seminal research in this field. • Kalea AZ, Schmidt AM, Hudson BI. RAGE: a novel biological and genetic marker for vascular disease. Clin Sci (Lond) 2009, 116:621–637. This study has had an important impact because it reviewed the role of RAGE in the pathogenesis of vascular disease and contains all the seminal research in this field.
13.
Zurück zum Zitat Osawa M, Yamamoto Y, Munesue S, et al. De-N-glycosylation or G82S mutation of RAGE sensitizes its interaction with advanced glycation endproducts. Biochim Biophys Acta. 2007;1770:1468–74.PubMed Osawa M, Yamamoto Y, Munesue S, et al. De-N-glycosylation or G82S mutation of RAGE sensitizes its interaction with advanced glycation endproducts. Biochim Biophys Acta. 2007;1770:1468–74.PubMed
14.
Zurück zum Zitat Leclerc E, Fritz G, Weibel M, Heizmann CW, Galichet A. S100B and S100A6 differentially modulate cell survival by interacting with distinct RAGE (receptor for advanced glycation end products) immunoglobulin domains. J Biol Chem. 2007;282:31317–31.PubMedCrossRef Leclerc E, Fritz G, Weibel M, Heizmann CW, Galichet A. S100B and S100A6 differentially modulate cell survival by interacting with distinct RAGE (receptor for advanced glycation end products) immunoglobulin domains. J Biol Chem. 2007;282:31317–31.PubMedCrossRef
15.
Zurück zum Zitat Hofmann MA, Drury S, Fu C, et al. RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides. Cell. 1999;97:889–901.PubMedCrossRef Hofmann MA, Drury S, Fu C, et al. RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides. Cell. 1999;97:889–901.PubMedCrossRef
16.
Zurück zum Zitat Hudson BI, Carter AM, Harja E, et al. Identification, classification, and expression of RAGE gene splice variants. FASEB J. 2008;22:1572–80.PubMedCrossRef Hudson BI, Carter AM, Harja E, et al. Identification, classification, and expression of RAGE gene splice variants. FASEB J. 2008;22:1572–80.PubMedCrossRef
17.
Zurück zum Zitat 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;25:1032–7.PubMedCrossRef 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;25:1032–7.PubMedCrossRef
18.
Zurück zum Zitat Zong H, Madden A, Ward M, Mooney MH, Elliott CT, Stitt AW. Homodimerization is essential for the receptor for advanced glycation end products (RAGE)-mediated signal transduction. J Biol Chem. 2010;285:23137–46.PubMedCrossRef Zong H, Madden A, Ward M, Mooney MH, Elliott CT, Stitt AW. Homodimerization is essential for the receptor for advanced glycation end products (RAGE)-mediated signal transduction. J Biol Chem. 2010;285:23137–46.PubMedCrossRef
19.
Zurück zum Zitat Yan SF, Ramasamy R, Bucciarelli LG, et al. RAGE and its ligands: a lasting memory in diabetic complications? Diab Vasc Dis Res. 2004;1:10–20.PubMedCrossRef Yan SF, Ramasamy R, Bucciarelli LG, et al. RAGE and its ligands: a lasting memory in diabetic complications? Diab Vasc Dis Res. 2004;1:10–20.PubMedCrossRef
20.
Zurück zum Zitat Hudson BI, Kalea AZ, Del Mar Arriero M, et al. Interaction of the RAGE cytoplasmic domain with diaphanous-1 is required for ligand-stimulated cellular migration through activation of Rac1 and Cdc42. J Biol Chem. 2008;283:34457–68.PubMedCrossRef Hudson BI, Kalea AZ, Del Mar Arriero M, et al. Interaction of the RAGE cytoplasmic domain with diaphanous-1 is required for ligand-stimulated cellular migration through activation of Rac1 and Cdc42. J Biol Chem. 2008;283:34457–68.PubMedCrossRef
21.
Zurück zum Zitat Xu Y, Toure F, Qu W, et al. Advanced glycation end product (AGE)-receptor for AGE (RAGE) signaling and up-regulation of Egr-1 in hypoxic macrophages. J Biol Chem. 2010;285:23233–40.PubMedCrossRef Xu Y, Toure F, Qu W, et al. Advanced glycation end product (AGE)-receptor for AGE (RAGE) signaling and up-regulation of Egr-1 in hypoxic macrophages. J Biol Chem. 2010;285:23233–40.PubMedCrossRef
22.
Zurück zum Zitat Takuma K, Fang F, Zhang W, et al. RAGE-mediated signaling contributes to intraneuronal transport of amyloid-beta and neuronal dysfunction. Proc Natl Acad Sci USA. 2009;106:20021–6.PubMed Takuma K, Fang F, Zhang W, et al. RAGE-mediated signaling contributes to intraneuronal transport of amyloid-beta and neuronal dysfunction. Proc Natl Acad Sci USA. 2009;106:20021–6.PubMed
23.
Zurück zum Zitat Huttunen HJ, Fages C, Rauvala H. Receptor for advanced glycation end products (RAGE)-mediated neurite outgrowth and activation of NF-kappaB require the cytoplasmic domain of the receptor but different downstream signaling pathways. J Biol Chem. 1999;274:19919–24.PubMedCrossRef Huttunen HJ, Fages C, Rauvala H. Receptor for advanced glycation end products (RAGE)-mediated neurite outgrowth and activation of NF-kappaB require the cytoplasmic domain of the receptor but different downstream signaling pathways. J Biol Chem. 1999;274:19919–24.PubMedCrossRef
24.
Zurück zum Zitat Bianchi R, Kastrisianaki E, Giambanco I, Donato R. S100B protein stimulates microglia migration via RAGE-dependent upregulation of chemokine expression and release. J Biol Chem 2011 Bianchi R, Kastrisianaki E, Giambanco I, Donato R. S100B protein stimulates microglia migration via RAGE-dependent upregulation of chemokine expression and release. J Biol Chem 2011
25.
Zurück zum Zitat Fosmark DS, Bragadottir R, Stene-Johansen I, et al. Increased vitreous levels of hydroimidazolone in type 2 diabetes patients are associated with retinopathy: a case-control study. Acta Ophthalmol Scand. 2007;85:618–22.PubMedCrossRef Fosmark DS, Bragadottir R, Stene-Johansen I, et al. Increased vitreous levels of hydroimidazolone in type 2 diabetes patients are associated with retinopathy: a case-control study. Acta Ophthalmol Scand. 2007;85:618–22.PubMedCrossRef
26.
Zurück zum Zitat Murata T, Nagai R, Ishibashi T, Inomuta H, Ikeda K, Horiuchi S. The relationship between accumulation of advanced glycation end products and expression of vascular endothelial growth factor in human diabetic retinas. Diabetologia. 1997;40:764–9.PubMedCrossRef Murata T, Nagai R, Ishibashi T, Inomuta H, Ikeda K, Horiuchi S. The relationship between accumulation of advanced glycation end products and expression of vascular endothelial growth factor in human diabetic retinas. Diabetologia. 1997;40:764–9.PubMedCrossRef
27.
Zurück zum Zitat Stitt AW, Bhaduri T, McMullen CB, Gardiner TA, Archer DB. Advanced glycation end products induce blood-retinal barrier dysfunction in normoglycemic rats. Mol Cell Biol Res Commun. 2000;3:380–8.PubMedCrossRef Stitt AW, Bhaduri T, McMullen CB, Gardiner TA, Archer DB. Advanced glycation end products induce blood-retinal barrier dysfunction in normoglycemic rats. Mol Cell Biol Res Commun. 2000;3:380–8.PubMedCrossRef
28.
Zurück zum Zitat Stitt AW, Curtis TM. Advanced glycation and retinal pathology during diabetes. Pharmacol Rep. 2005;57(Suppl):156–68.PubMed Stitt AW, Curtis TM. Advanced glycation and retinal pathology during diabetes. Pharmacol Rep. 2005;57(Suppl):156–68.PubMed
29.
Zurück zum Zitat Barile GR, Pachydaki SI, Tari SR, et al. The RAGE axis in early diabetic retinopathy. Invest Ophthalmol Vis Sci. 2005;46:2916–24.PubMedCrossRef Barile GR, Pachydaki SI, Tari SR, et al. The RAGE axis in early diabetic retinopathy. Invest Ophthalmol Vis Sci. 2005;46:2916–24.PubMedCrossRef
30.
Zurück zum Zitat •• Zong H, Ward M, Madden A, et al.. Hyperglycaemia-induced pro-inflammatory responses by retinal Muller glia are regulated by the receptor for advanced glycation end-products (RAGE). Diabetologia 2010, 53:2656–2666. This paper demonstrated that RAGE interaction with its ligands plays an important role in retinal glial dysfunction during diabetic retinopathy. RAGE and its ligand S100B were induced by hyperglycemia in Müller glia, in vitro and in vivo. The early induction of S100B/RAGE expression by hyperglycemia in Muller glia results in the elevated levels of proinflammatory cytokines including VEGF and MCP-1, which are key mediators for diabetic retinopathy. This response can be attenuated by sRAGE or RAGE small interfering RNA, implicating the critical role of RAGE in the initiation of diabetic retinopathy. •• Zong H, Ward M, Madden A, et al.. Hyperglycaemia-induced pro-inflammatory responses by retinal Muller glia are regulated by the receptor for advanced glycation end-products (RAGE). Diabetologia 2010, 53:2656–2666. This paper demonstrated that RAGE interaction with its ligands plays an important role in retinal glial dysfunction during diabetic retinopathy. RAGE and its ligand S100B were induced by hyperglycemia in Müller glia, in vitro and in vivo. The early induction of S100B/RAGE expression by hyperglycemia in Muller glia results in the elevated levels of proinflammatory cytokines including VEGF and MCP-1, which are key mediators for diabetic retinopathy. This response can be attenuated by sRAGE or RAGE small interfering RNA, implicating the critical role of RAGE in the initiation of diabetic retinopathy.
31.
Zurück zum Zitat • Yao D, Brownlee M. Hyperglycemia-induced reactive oxygen species increase expression of the receptor for advanced glycation end products (RAGE) and RAGE ligands. Diabetes 2010, 59:249–255. This paper is important because it evaluated the induction of RAGE and its ligands, S100A8, S100A12, and HMGB1, in human aortic endothelial cells and indicated modulation by ROS. This suggests that ROS cannot only be induced as the end point of RAGE activation, but also act as a positive feedback of RAGE-mediated proinflammatory signaling. • Yao D, Brownlee M. Hyperglycemia-induced reactive oxygen species increase expression of the receptor for advanced glycation end products (RAGE) and RAGE ligands. Diabetes 2010, 59:249–255. This paper is important because it evaluated the induction of RAGE and its ligands, S100A8, S100A12, and HMGB1, in human aortic endothelial cells and indicated modulation by ROS. This suggests that ROS cannot only be induced as the end point of RAGE activation, but also act as a positive feedback of RAGE-mediated proinflammatory signaling.
32.
Zurück zum Zitat Fletcher EL, Phipps JA, Ward MM, Puthussery T, Wilkinson-Berka JL. Neuronal and glial cell abnormality as predictors of progression of diabetic retinopathy. Curr Pharm Des. 2007;13:2699–712.PubMedCrossRef Fletcher EL, Phipps JA, Ward MM, Puthussery T, Wilkinson-Berka JL. Neuronal and glial cell abnormality as predictors of progression of diabetic retinopathy. Curr Pharm Des. 2007;13:2699–712.PubMedCrossRef
33.
Zurück zum Zitat Hirata C, Nakano K, Nakamura N, et al. Advanced glycation end products induce expression of vascular endothelial growth factor by retinal Muller cells. Biochem Biophys Res Commun. 1997;236:712–15.PubMedCrossRef Hirata C, Nakano K, Nakamura N, et al. Advanced glycation end products induce expression of vascular endothelial growth factor by retinal Muller cells. Biochem Biophys Res Commun. 1997;236:712–15.PubMedCrossRef
34.
Zurück zum Zitat Lieth E, Barber AJ, Xu B, et al. Glial reactivity and impaired glutamate metabolism in short-term experimental diabetic retinopathy. Penn State Retina Research Group. Diabetes. 1998;47:815–20.PubMedCrossRef Lieth E, Barber AJ, Xu B, et al. Glial reactivity and impaired glutamate metabolism in short-term experimental diabetic retinopathy. Penn State Retina Research Group. Diabetes. 1998;47:815–20.PubMedCrossRef
35.
Zurück zum Zitat Curtis TM, Hamilton R, Yong PH, et al. Muller glial dysfunction during diabetic retinopathy in rats is linked to accumulation of advanced glycation end-products and advanced lipoxidation end-products. Diabetologia. 2011;54:690–8.PubMedCrossRef Curtis TM, Hamilton R, Yong PH, et al. Muller glial dysfunction during diabetic retinopathy in rats is linked to accumulation of advanced glycation end-products and advanced lipoxidation end-products. Diabetologia. 2011;54:690–8.PubMedCrossRef
36.
Zurück zum Zitat Donato R. S100: a multigenic family of calcium-modulated proteins of the EF-hand type with intracellular and extracellular functional roles. Int J Biochem Cell Biol. 2001;33:637–68.PubMedCrossRef Donato R. S100: a multigenic family of calcium-modulated proteins of the EF-hand type with intracellular and extracellular functional roles. Int J Biochem Cell Biol. 2001;33:637–68.PubMedCrossRef
37.
Zurück zum Zitat Mills CD, Kincaid K, Alt JM, Heilman MJ, Hill AM. M-1/M-2 macrophages and the Th1/Th2 paradigm. J Immunol. 2000;164:6166–73.PubMed Mills CD, Kincaid K, Alt JM, Heilman MJ, Hill AM. M-1/M-2 macrophages and the Th1/Th2 paradigm. J Immunol. 2000;164:6166–73.PubMed
38.
Zurück zum Zitat Schalkwijk CG, Ligtvoet N, Twaalfhoven H, et al. Amadori albumin in type 1 diabetic patients: correlation with markers of endothelial function, association with diabetic nephropathy, and localization in retinal capillaries. Diabetes. 1999;48:2446–53.PubMedCrossRef Schalkwijk CG, Ligtvoet N, Twaalfhoven H, et al. Amadori albumin in type 1 diabetic patients: correlation with markers of endothelial function, association with diabetic nephropathy, and localization in retinal capillaries. Diabetes. 1999;48:2446–53.PubMedCrossRef
39.
Zurück zum Zitat Moore TC, Moore JE, Kaji Y, et al. The role of advanced glycation end products in retinal microvascular leukostasis. Invest Ophthalmol Vis Sci. 2003;44:4457–64.PubMedCrossRef Moore TC, Moore JE, Kaji Y, et al. The role of advanced glycation end products in retinal microvascular leukostasis. Invest Ophthalmol Vis Sci. 2003;44:4457–64.PubMedCrossRef
40.
Zurück zum Zitat Chen BH, Jiang DY, Tang LS. Advanced glycation end-products induce apoptosis involving the signaling pathways of oxidative stress in bovine retinal pericytes. Life Sci. 2006;79:1040–8.PubMedCrossRef Chen BH, Jiang DY, Tang LS. Advanced glycation end-products induce apoptosis involving the signaling pathways of oxidative stress in bovine retinal pericytes. Life Sci. 2006;79:1040–8.PubMedCrossRef
41.
Zurück zum Zitat Foulds WS. The choroidal circulation and retinal metabolism–an overview. Eye (Lond). 1990;4(Pt 2):243–8. Foulds WS. The choroidal circulation and retinal metabolism–an overview. Eye (Lond). 1990;4(Pt 2):243–8.
42.
Zurück zum Zitat Lu M, Kuroki M, Amano S, et al. Advanced glycation end products increase retinal vascular endothelial growth factor expression. J Clin Invest. 1998;101:1219–24.PubMedCrossRef Lu M, Kuroki M, Amano S, et al. Advanced glycation end products increase retinal vascular endothelial growth factor expression. J Clin Invest. 1998;101:1219–24.PubMedCrossRef
43.
Zurück zum Zitat Yamagishi S, Nakamura K, Matsui T, et al. Pigment epithelium-derived factor inhibits advanced glycation end product-induced retinal vascular hyperpermeability by blocking reactive oxygen species-mediated vascular endothelial growth factor expression. J Biol Chem. 2006;281:20213–20.PubMedCrossRef Yamagishi S, Nakamura K, Matsui T, et al. Pigment epithelium-derived factor inhibits advanced glycation end product-induced retinal vascular hyperpermeability by blocking reactive oxygen species-mediated vascular endothelial growth factor expression. J Biol Chem. 2006;281:20213–20.PubMedCrossRef
44.
Zurück zum Zitat Sheikpranbabu S, Haribalaganesh R, Lee KJ, Gurunathan S. Pigment epithelium-derived factor inhibits advanced glycation end products-induced retinal vascular permeability. Biochimie. 2010;92:1040–51.PubMedCrossRef Sheikpranbabu S, Haribalaganesh R, Lee KJ, Gurunathan S. Pigment epithelium-derived factor inhibits advanced glycation end products-induced retinal vascular permeability. Biochimie. 2010;92:1040–51.PubMedCrossRef
45.
Zurück zum Zitat Nitti M, Furfaro AL, Traverso N, et al. PKC delta and NADPH oxidase in AGE-induced neuronal death. Neurosci Lett. 2007;416:261–5.PubMedCrossRef Nitti M, Furfaro AL, Traverso N, et al. PKC delta and NADPH oxidase in AGE-induced neuronal death. Neurosci Lett. 2007;416:261–5.PubMedCrossRef
46.
Zurück zum Zitat Wang Y, Vom Hagen F, Pfister F, et al. Receptor for advanced glycation end product expression in experimental diabetic retinopathy. Ann NY Acad Sci. 2008;1126:42–5.PubMedCrossRef Wang Y, Vom Hagen F, Pfister F, et al. Receptor for advanced glycation end product expression in experimental diabetic retinopathy. Ann NY Acad Sci. 2008;1126:42–5.PubMedCrossRef
47.
Zurück zum Zitat Hammes HP, Martin S, Federlin K, Geisen K, Brownlee M. Aminoguanidine treatment inhibits the development of experimental diabetic retinopathy. Proc Natl Acad Sci USA. 1991;88:11555–8.PubMedCrossRef Hammes HP, Martin S, Federlin K, Geisen K, Brownlee M. Aminoguanidine treatment inhibits the development of experimental diabetic retinopathy. Proc Natl Acad Sci USA. 1991;88:11555–8.PubMedCrossRef
48.
Zurück zum Zitat Canning P, Glenn JV, Hsu DK, Liu FT, Gardiner TA, Stitt AW. Inhibition of advanced glycation and absence of galectin-3 prevent blood-retinal barrier dysfunction during short-term diabetes. Exp Diabetes Res. 2007;2007:51837.PubMed Canning P, Glenn JV, Hsu DK, Liu FT, Gardiner TA, Stitt AW. Inhibition of advanced glycation and absence of galectin-3 prevent blood-retinal barrier dysfunction during short-term diabetes. Exp Diabetes Res. 2007;2007:51837.PubMed
49.
Zurück zum Zitat Yatoh S, Mizutani M, Yokoo T, et al. Antioxidants and an inhibitor of advanced glycation ameliorate death of retinal microvascular cells in diabetic retinopathy. Diabetes Metab Res Rev. 2006;22:38–45.PubMedCrossRef Yatoh S, Mizutani M, Yokoo T, et al. Antioxidants and an inhibitor of advanced glycation ameliorate death of retinal microvascular cells in diabetic retinopathy. Diabetes Metab Res Rev. 2006;22:38–45.PubMedCrossRef
50.
Zurück zum Zitat Bhatwadekar A, Glenn JV, Figarola JL, et al. A new advanced glycation inhibitor, LR-90, prevents experimental diabetic retinopathy in rats. Br J Ophthalmol. 2008;92:545–7.PubMedCrossRef Bhatwadekar A, Glenn JV, Figarola JL, et al. A new advanced glycation inhibitor, LR-90, prevents experimental diabetic retinopathy in rats. Br J Ophthalmol. 2008;92:545–7.PubMedCrossRef
51.
Zurück zum Zitat Kaji Y, Usui T, Ishida S, et al. Inhibition of diabetic leukostasis and blood-retinal barrier breakdown with a soluble form of a receptor for advanced glycation end products. Invest Ophthalmol Vis Sci. 2007;48:858–65.PubMedCrossRef Kaji Y, Usui T, Ishida S, et al. Inhibition of diabetic leukostasis and blood-retinal barrier breakdown with a soluble form of a receptor for advanced glycation end products. Invest Ophthalmol Vis Sci. 2007;48:858–65.PubMedCrossRef
52.
Zurück zum Zitat Chen Y, Akirav EM, Chen W, et al. RAGE ligation affects T cell activation and controls T cell differentiation. J Immunol. 2008;181:4272–8.PubMed Chen Y, Akirav EM, Chen W, et al. RAGE ligation affects T cell activation and controls T cell differentiation. J Immunol. 2008;181:4272–8.PubMed
53.
Zurück zum Zitat Sabbagh MN, Agro A, Bell J, Aisen PS, Schweizer E, Galasko D. PF-04494700, an Oral Inhibitor of Receptor for Advanced Glycation End Products (RAGE), in Alzheimer Disease. Alzheimer Dis Assoc Disord 2010 Sabbagh MN, Agro A, Bell J, Aisen PS, Schweizer E, Galasko D. PF-04494700, an Oral Inhibitor of Receptor for Advanced Glycation End Products (RAGE), in Alzheimer Disease. Alzheimer Dis Assoc Disord 2010
54.
Zurück zum Zitat Yamamoto K, Kitayama W, Denda A, Sasahira T, Kuniyasu H, Kirita T. Expression of receptor for advanced glycation end products during rat tongue carcinogenesis by 4-nitroquinoline 1-oxide and effect of a selective cyclooxygenase-2 inhibitor, etodolac. Pathobiology. 2006;73:317–24.PubMedCrossRef Yamamoto K, Kitayama W, Denda A, Sasahira T, Kuniyasu H, Kirita T. Expression of receptor for advanced glycation end products during rat tongue carcinogenesis by 4-nitroquinoline 1-oxide and effect of a selective cyclooxygenase-2 inhibitor, etodolac. Pathobiology. 2006;73:317–24.PubMedCrossRef
55.
Zurück zum Zitat Yamagishi S, Matsui T, Nakamura K, et al. Olmesartan blocks inflammatory reactions in endothelial cells evoked by advanced glycation end products by suppressing generation of reactive oxygen species. Ophthalmic Res. 2008;40:10–5.PubMedCrossRef Yamagishi S, Matsui T, Nakamura K, et al. Olmesartan blocks inflammatory reactions in endothelial cells evoked by advanced glycation end products by suppressing generation of reactive oxygen species. Ophthalmic Res. 2008;40:10–5.PubMedCrossRef
56.
Zurück zum Zitat Marx N, Walcher D, Ivanova N, et al. Thiazolidinediones reduce endothelial expression of receptors for advanced glycation end products. Diabetes. 2004;53:2662–8.PubMedCrossRef Marx N, Walcher D, Ivanova N, et al. Thiazolidinediones reduce endothelial expression of receptors for advanced glycation end products. Diabetes. 2004;53:2662–8.PubMedCrossRef
57.
Zurück zum Zitat Yamagishi S, Takeuchi M. Nifedipine inhibits gene expression of receptor for advanced glycation end products (RAGE) in endothelial cells by suppressing reactive oxygen species generation. Drugs Exp Clin Res. 2004;30:169–75.PubMed Yamagishi S, Takeuchi M. Nifedipine inhibits gene expression of receptor for advanced glycation end products (RAGE) in endothelial cells by suppressing reactive oxygen species generation. Drugs Exp Clin Res. 2004;30:169–75.PubMed
58.
Zurück zum Zitat Praidou A, Androudi S, Brazitikos P, Karakiulakis G, Papakonstantinou E, Dimitrakos S. Angiogenic growth factors and their inhibitors in diabetic retinopathy. Curr Diabetes Rev. 2010;6:304–12.PubMedCrossRef Praidou A, Androudi S, Brazitikos P, Karakiulakis G, Papakonstantinou E, Dimitrakos S. Angiogenic growth factors and their inhibitors in diabetic retinopathy. Curr Diabetes Rev. 2010;6:304–12.PubMedCrossRef
59.
Zurück zum Zitat Abdallah W, Fawzi AA. Anti-VEGF therapy in proliferative diabetic retinopathy. Int Ophthalmol Clin. 2009;49:95–107.PubMedCrossRef Abdallah W, Fawzi AA. Anti-VEGF therapy in proliferative diabetic retinopathy. Int Ophthalmol Clin. 2009;49:95–107.PubMedCrossRef
60.
Zurück zum Zitat Gaudreault J, Fei D, Rusit J, Suboc P, Shiu V. Preclinical pharmacokinetics of Ranibizumab (rhuFabV2) after a single intravitreal administration. Invest Ophthalmol Vis Sci. 2005;46:726–33.PubMedCrossRef Gaudreault J, Fei D, Rusit J, Suboc P, Shiu V. Preclinical pharmacokinetics of Ranibizumab (rhuFabV2) after a single intravitreal administration. Invest Ophthalmol Vis Sci. 2005;46:726–33.PubMedCrossRef
61.
Zurück zum Zitat Ferrara N, Hillan KJ, Gerber HP, Novotny W. Discovery and development of bevacizumab, an anti-VEGF antibody for treating cancer. Nat Rev Drug Discov. 2004;3:391–400.PubMedCrossRef Ferrara N, Hillan KJ, Gerber HP, Novotny W. Discovery and development of bevacizumab, an anti-VEGF antibody for treating cancer. Nat Rev Drug Discov. 2004;3:391–400.PubMedCrossRef
62.
Zurück zum Zitat Arevalo JF, Maia M, Flynn Jr HW, et al. Tractional retinal detachment following intravitreal bevacizumab (Avastin) in patients with severe proliferative diabetic retinopathy. Br J Ophthalmol. 2008;92:213–16.PubMedCrossRef Arevalo JF, Maia M, Flynn Jr HW, et al. Tractional retinal detachment following intravitreal bevacizumab (Avastin) in patients with severe proliferative diabetic retinopathy. Br J Ophthalmol. 2008;92:213–16.PubMedCrossRef
63.
Zurück zum Zitat Zhao LQ, Zhu H, Zhao PQ, Hu YQ. A systematic review and meta-analysis of clinical outcomes of vitrectomy with or without intravitreal bevacizumab pretreatment for severe diabetic retinopathy. Br J Ophthalmol 2011. Zhao LQ, Zhu H, Zhao PQ, Hu YQ. A systematic review and meta-analysis of clinical outcomes of vitrectomy with or without intravitreal bevacizumab pretreatment for severe diabetic retinopathy. Br J Ophthalmol 2011.
64.
Zurück zum Zitat Kim OS, Kim J, Kim CS, Kim NH, Kim JS. KIOM-79 prevents methyglyoxal-induced retinal pericyte apoptosis in vitro and in vivo. J Ethnopharmacol. 2010;129:285–92.PubMedCrossRef Kim OS, Kim J, Kim CS, Kim NH, Kim JS. KIOM-79 prevents methyglyoxal-induced retinal pericyte apoptosis in vitro and in vivo. J Ethnopharmacol. 2010;129:285–92.PubMedCrossRef
65.
Zurück zum Zitat Wang Q, Pfister F, Dorn-Beineke A, et al. Low-dose erythropoietin inhibits oxidative stress and early vascular changes in the experimental diabetic retina. Diabetologia. 2010;53:1227–38.PubMedCrossRef Wang Q, Pfister F, Dorn-Beineke A, et al. Low-dose erythropoietin inhibits oxidative stress and early vascular changes in the experimental diabetic retina. Diabetologia. 2010;53:1227–38.PubMedCrossRef
66.
Zurück zum Zitat Yamagishi S, Nakamura K, Matsui T, Takeuchi M. Minodronate, a nitrogen-containing bisphosphonate, is a promising remedy for treating patients with diabetic retinopathy. Med Hypotheses. 2006;66:273–5.PubMedCrossRef Yamagishi S, Nakamura K, Matsui T, Takeuchi M. Minodronate, a nitrogen-containing bisphosphonate, is a promising remedy for treating patients with diabetic retinopathy. Med Hypotheses. 2006;66:273–5.PubMedCrossRef
67.
Zurück zum Zitat Kowluru RA, Kanwar M, Chan PS, Zhang JP. Inhibition of retinopathy and retinal metabolic abnormalities in diabetic rats with AREDS-based micronutrients. Arch Ophthalmol. 2008;126:1266–72.PubMedCrossRef Kowluru RA, Kanwar M, Chan PS, Zhang JP. Inhibition of retinopathy and retinal metabolic abnormalities in diabetic rats with AREDS-based micronutrients. Arch Ophthalmol. 2008;126:1266–72.PubMedCrossRef
Metadaten
Titel
AGEs, RAGE, and Diabetic Retinopathy
verfasst von
Hongliang Zong
Micheal Ward
Alan W. Stitt
Publikationsdatum
01.08.2011
Verlag
Current Science Inc.
Erschienen in
Current Diabetes Reports / Ausgabe 4/2011
Print ISSN: 1534-4827
Elektronische ISSN: 1539-0829
DOI
https://doi.org/10.1007/s11892-011-0198-7

Weitere Artikel der Ausgabe 4/2011

Current Diabetes Reports 4/2011 Zur Ausgabe

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.