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糖化终末产物与氧化应激及血管病变 被引量：4

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摘要 葡萄糖与含氨基生物分子（主要为蛋白质，也包括核酸和脂类）可发生复杂的反应，最后形成一类结构复杂的化合物，称为糖化终末产物fadvancedglycationendproducts，AGEs）。AGEs结构极为复杂，与很多病理生理过程密切相关。
作者 苏青
机构地区 上海交通大学医学院附属新华医院内分泌科
出处 《内科理论与实践》 2012年第3期152-155,共4页 Journal of Internal Medicine Concepts & Practice
关键词 糖化终末产物 氧化应激 血管病变
分类号 R587.1 [医药卫生—内分泌] R587.2 [医药卫生—内分泌]
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参考文献18

  • 1王瑞良,苏青.RAGE及其配体的临床意义研究进展[J].国际内分泌代谢杂志,2006,26(3):160-162. 被引量：23
  • 2Giacco F, Brownlee M. Oxidative stress and diabetic complications[J]. Circ Res, 2010, 107(9): 1058-1070.
  • 3葛勤敏,边帆,许勤,苏青.糖化终末产物对内皮细胞氧化应激的影响[J].上海交通大学学报（医学版）,2007,27(2):178-181. 被引量：6
  • 4Ge QM, Dong Y, Su Q. Effects of glucose and advanced glycation end products on oxidative stress in MIN6 cells [J]. Cell Mol Biol (Noisy-le-grand), 2010, 56 Suppl: OL1231-OL1238.
  • 5杜世春,林宁,葛勤敏,简蔚霞,董艳,苏青.糖化终末产物对MIN6细胞活力及活性氧（ROS）水平的影响[J].中华内分泌代谢杂志,2011,27(2):152-154. 被引量：5
  • 6Lin N, Zhang H, Su Q. Advanced glycation end-products induce injury to pancreatic 15 cells through oxidative stress[J]. Diabetes Metab, 2012. [Epub ahead of print].
  • 7Reiniger N, Lau K, McCalla D, et al. Deletion of the receptor for advanced glycation end products reduces glo- merulosclerosis and preserves renal function in the dia-betic OVE26 mouse[J]. Diabetes, 2010, 59(8): 2043-2054.
  • 8Sheikpranbabu S, Haribalaganesh R, Gurunathan S. Pigment epithelium-derived factor inhibits advanced glyeation end-products-induced cytotoxicity in retinal pericytes[J]. Diabetes Metab, 2011, 37(6): 505-511.
  • 9Sheikpranbabu S, Haribalaganesh R, Banumathi E, et al. Pigment epithelium-derived factor inhibits advanced gly- cation end-product-induced angiogenesis and stimulates apoptosis in retinal endothelial cells [J]. Life Sci, 2009, 85(21-22): 719-731.
  • 10Ide Y, Matsui T, Ishibashi Y, et al. Pigment epithelium- derived factor inhibits advanced glycation end product- elicited mesangial cell damage by blocking NF-KB acti- vation[J]. Microvasc Res, 2010, 80(2): 227-232.

二级参考文献31

  • 1Yamagishi S.Advanced glycation end products and receptor-oxidative stress system in diabetic vascular complications.Ther Apher Dial,2009,13,6:534-539.
  • 2Yan SF,Barile GR,D' Agati V,et al.The biology of RAGE and its ligands:uncovering mechanisms at the heart of diabetes and its complications.Curr Diab Rep,2007,7:146-153.
  • 3Yan SF,Yan SD,Herold K,et al.Receptor for advanced glycation end products and the cardiovascular complications of diabetes and beyond:lessons from ageing.Endocrinol Metab Clin North Am,2006,35:511-524.
  • 4Lim M,Park L,Shin G,et al.Induction of apoptosis of β cells of the pancreas by advanced glycation end-products,important mediators of chronic complications of diabetes mellitus.Ann N Y Acad Sci,2008,1150:311-315.
  • 5Luciano Viviani G,Puddu A,Sacchi G,et al.Glycated fetal calf serum affects the viability of an insulin-secreting cell line in vitro.Metabolism,2008,57:163-169.
  • 6Fenster BE,Tsao PS,Rockson SG.Endothelial dysfunction:clinical strategies for treating oxidant stress.Am Heart J,2003,146,2:218-226.
  • 7Schmitt A,Bigl K,Meiners I,et al.Induction of reactive oxygen species and cell survival in the presence of advanced glycation end products and similar structures.Biochim Biophys Acta,2006,1763,9:927-936.
  • 8Forbes JM, Thallas V, Thomas MC, et al. The breakdown of preexisting advanced glycation end products is associated with reduced renal fibrosis in experimental diabetes. FASEB J, 2003,17 : 1762-1764.
  • 9Candido R, Forbes JM, Thomas MC, et al. A breaker of advanced glycation end products attenuates diabetes-induced myocardial structural changes: Circ Res, 2003,92:785-792.
  • 10Haslbeck KM, Schleieher E, Bierhaus A, et al. The AGEVRAGE/NF-kappaB pathway may contribute to the pathogenesis of polyneuropathy in impaired glucose tolerance (IGT). Exp Clin Endocrinol Diabetes,2005,113 : 288-291.

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内科理论与实践
2012年 第3期

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