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晚期糖基化终产物在动脉粥样硬化中的作用 被引量：4

Advanced glycation end products: modulators in diabetes accelerated atherosclerosis
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摘要 2型糖尿病患者动脉粥样硬化的发病率明显增高。糖尿病通过增加常规的危险因素(如血脂异常、高血压)或糖尿病特有的危险因子(如晚期糖基化终产物AGEs),促进动脉粥样硬化的发展。AGEs作为蛋白质或脂质与还原糖糖基化的终产物,在血管细胞中通过与RAGE结合促进炎症因子的表达,参与动脉粥样硬化的发展。近年来,关于AGEs及其受体(RAGE)对糖尿病动脉粥样硬化影响的研究较为深入。本文旨在对近年来有关AGEs/RAGE在糖尿病加速的动脉粥样硬化中作用的研究进展作一综述。 There is an increased morbidity of atherosclerosis in patients with type 2 diabetes. Diabetes may be associated with accelerated atherosclerosis by either increasing the conventional risk factors, such as dyslipidemia and high blood pressure, or diabetic-specific risk factor, such as advanced glycation end products （AGEs）. AGEs are proteins or lipids that become glycated after exposure to sugars. By engaging in the RAGE, AGEs induce the expression of proinflammatory mediators in various vascular cell types. In recent years, further studies have shown the association between AGEs and RAGE in diabetes accelerated atherosclerosis. The following review will discuss the potential role of the advanced AGEs-RAGE axis in diabetes-accelerated atherosclerosis as a mediator in lesion development in patients with type 2 diabetes.
作者 贺艳红 袁晓晨 张振刚
机构地区 扬州大学第二附属医院心内科
出处 《中华临床医师杂志（电子版）》 CAS 2014年第5期81-84,共4页 Chinese Journal of Clinicians(Electronic Edition)
基金 国家自然科学基金(81270198) 扬州市科技项目(YZ2012130)
关键词 糖基化终产物 高级 动脉粥样硬化 糖尿病 晚期糖基化终产物受体 Glycosylation end products,advanced Atherosclerosis Diabetes mellitus Receptor for advanced glycation end products
分类号 R543 [医药卫生—心血管疾病]
  • 相关文献

参考文献27

  • 1MarK R, Bermejo JL, Bierhans A,et al. The receptor glycation end peoducts is dispensable in a mouse model of oral and esophageal carcinogenesis[J]. Histol Histopathol, 2013, 28(12): 1585-1594.
  • 2Danzaki K, Matsui Y, Ikesue M,et al. Interleuldn-17A deficiency accelerates unstable atherosclerotic plaque ftmnafion in apolipoprotein E-deficient mice[J]. Arterioscler Thromb Vasc Biol, 2012, 32(2): 273-280.
  • 3Kanauchi M, Tsujimoto N, Hashimoto T. Advanced glycation end products in nondiabetic patients with coronary artery disease[J]. Diabetic Care, 2001, 24(9): 1620-1623.
  • 4Yamagishi S, Matsui T, Ueda S, et al. Advanced glyeation end products (AGEs) and cardiovascular disease (CVD) in diabetes[J]. Cardiovasc Hematol Agents Med Chem, 2007, 5(3): 236-240.
  • 5Stratton IM, Adler AI, Neil HA, et al. Association of glyeaemia with maerovaseular and mierovaseular complications of type 2 diabetes (UKPDS 35): prospective observational study[J]. Br Ivied J, 2000,321(7258): 405-412.
  • 6Junghyun Kim, Ki Mo Kim, Chau-Sik Kim,et al. Puerarin inhibits the retinal pericyte apoptosis induced by advanced glycation end products in vitro and in vivo by inhibiting NADPH oxidase-related oxidative stress[J]. Free Radial Biology and Medicine, 2012, 53(2): 357-365.
  • 7Bondeva T, Heinzig J, Ruhe C, et al. Advanced glycated end-products affect hif-trenseriptional activity in renal eells[J].Mol Endocrinol, 2013, 27: 1918-1933.
  • 8Forbes JM, Cooper ME. Mechanisms of diabetic complications[J]. Physiol Rev, 2013, 93(1): 137-188.
  • 9Ando R, Ueda S, Yamagishi S, et al. Involvemont of adverted glyeatien end product-induced asymmetric dimetliylarginine generation in endothelial dysfunction[J]. Diab Vase Dis Res, 2013, 10(6): 436-441.
  • 10Crilchrist M, Wmyard PG Aizawa K, ot al. Effect of dietary nitrate on blood pressure, endothelial function, and insulin sensitivity in type 2 diabetes[J]. Free Radic Biol Meal, 2013, 60: 89-97.

二级参考文献27

  • 1MarK R, Bermejo JL, Bierhans A,et al. The receptor glycation end peoducts is dispensable in a mouse model of oral and esophageal carcinogenesis[J]. Histol Histopathol, 2013, 28(12): 1585-1594.
  • 2Danzaki K, Matsui Y, Ikesue M,et al. Interleuldn-17A deficiency accelerates unstable atherosclerotic plaque ftmnafion in apolipoprotein E-deficient mice[J]. Arterioscler Thromb Vasc Biol, 2012, 32(2): 273-280.
  • 3Kanauchi M, Tsujimoto N, Hashimoto T. Advanced glycation end products in nondiabetic patients with coronary artery disease[J]. Diabetic Care, 2001, 24(9): 1620-1623.
  • 4Yamagishi S, Matsui T, Ueda S, et al. Advanced glyeation end products (AGEs) and cardiovascular disease (CVD) in diabetes[J]. Cardiovasc Hematol Agents Med Chem, 2007, 5(3): 236-240.
  • 5Stratton IM, Adler AI, Neil HA, et al. Association of glyeaemia with maerovaseular and mierovaseular complications of type 2 diabetes (UKPDS 35): prospective observational study[J]. Br Ivied J, 2000,321(7258): 405-412.
  • 6Junghyun Kim, Ki Mo Kim, Chau-Sik Kim,et al. Puerarin inhibits the retinal pericyte apoptosis induced by advanced glycation end products in vitro and in vivo by inhibiting NADPH oxidase-related oxidative stress[J]. Free Radial Biology and Medicine, 2012, 53(2): 357-365.
  • 7Bondeva T, Heinzig J, Ruhe C, et al. Advanced glycated end-products affect hif-trenseriptional activity in renal eells[J].Mol Endocrinol, 2013, 27: 1918-1933.
  • 8Forbes JM, Cooper ME. Mechanisms of diabetic complications[J]. Physiol Rev, 2013, 93(1): 137-188.
  • 9Ando R, Ueda S, Yamagishi S, et al. Involvemont of adverted glyeatien end product-induced asymmetric dimetliylarginine generation in endothelial dysfunction[J]. Diab Vase Dis Res, 2013, 10(6): 436-441.
  • 10Crilchrist M, Wmyard PG Aizawa K, ot al. Effect of dietary nitrate on blood pressure, endothelial function, and insulin sensitivity in type 2 diabetes[J]. Free Radic Biol Meal, 2013, 60: 89-97.

共引文献3

同被引文献79

引证文献4

二级引证文献23

中华临床医师杂志（电子版）
2014年 第5期

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