期刊文献+

活性氧与糖基化终产物致动脉粥样硬化作用的关系 被引量:3

Interaction of reactive oxygen species in atherogenetic properties of advanced glycation end products in diabetes
下载PDF
导出
摘要 There is overwhelming evidence for an involvement of reactive oxygen species(ROS) in the pathogenesis of atherosclerosis(AS) in diabetes mellitus(DM). For many years, knowledge on the contribution to diabetic complications and vascular disease induced by advanced glycation end-products(AGEs)has been rising. During the development of atherosclerosis, AGEs and ROS might have interaction. In this article, we provided four angles of view to discuss the role of ROS in the pathogenesis of atherosclerosis: the chemistry of ROS, the effect of vascular targets of ROS on activity of AGEs, the role of ROS in the pathogenesis of atherogenesis by AGEs, the same effect of ROS and AGEs-transcriptional regulation. [ There is overwhelming evidence for an involvement of reactive oxygen species(ROS) in the pathogenesis of atherosclerosis(AS) in diabetes mellitus(DM). For many years, knowledge on the contribution to diabetic complications and vascular disease induced by advanced glycation end-products(AGEs)has been rising. During the development of atherosclerosis, AGEs and ROS might have interaction. In this article, we provided four angles of view to discuss the role of ROS in the pathogenesis of atherosclerosis: the chemistry of ROS, the effect of vascular targets of ROS on activity of AGEs, the role of ROS in the pathogenesis of atherogenesis by AGEs, the same effect of ROS and AGEs-transcriptional regulation. [
作者 冯 刘乃丰
出处 《中国病理生理杂志》 CAS CSCD 北大核心 2003年第12期1705-1708,共4页 Chinese Journal of Pathophysiology
关键词 活性氧 动脉硬化 糖尿病 Reactive oxygen species Arteriosclerosis Diabetes mellitus
  • 相关文献

参考文献15

  • 1[1]Sorescu D, Weiss D, Lassegue V, et al. Superoxide production and expression of NOX family proteins in human atherosclerosis [J]. Circulation,2002,105(12):1429- 1435.
  • 2[2]Leunda Casi A, Genicot G, Pampfer S, et al. Increased cell death in mouse balstocysts exposed to high D - glucose in vitro: implications of an oxidative stress and alterations in glucose metabolism[J]. Diabetologia,2002,45(4) :571 - 579.
  • 3[3]Zill H, Gunther R, Erbersdobler HF, et al. RAGE expression and AGE - induced MAP kinase activation in Caco - 2 cells [J]. Biochem Biophys Res Commun,2001,288(5): 1108-1124.
  • 4[4]Cuda G, Patemo R, Ceravolo R, et al. Protection of human endothelial cells from oxidative stress :role of Ras - ERK1/2 signaling[J]. Circulation,2002,105(8) :968 - 974.
  • 5[5]Yamagishi SI, Edelstein D, Du XL, et al. Hyperglycemia potentiates collagen - induced platelet activation through mitochondrial superoxide overproduction [ J ]. Diabetes, 2001, 50(6): 1491 - 1494.
  • 6[6]Yim MB, Yim HS, Lee C,et al. Proteinglycation: creationof catalytic sites for free radical generation[J]. Ann N Y Acad Sci,2001,928: 48-53.
  • 7[7]Idris I, Gray S, Donnelly R. Protein kinase C activation:isozyme- specific effects on metabolism and cardiovascular complications in diabetes[J]. Diabetologia,2001,44(6):659- 673.
  • 8[8]Uemura S, Matsushita H, Li W, et al. Diabetes mellitus enhances vascular matrix metalloproteinase activity: role of oxidative stress[J]. Circ Res,2001,88(12): 1291 - 1298.
  • 9[9]Golovchenko I,G oalstone ML,Watson P,et al. Hyperinsulinemia enhances transcriptional activity of nuclear factor- kappa B induced by angiotensin Ⅱ, hyperglycemia, and advanced glycosylation end products in vascular smooth muscle cells[J].Circ Res, 2000,87(9):746-752.
  • 10[10]Garcia Soriano F,Virag L,Jagtap P,et al. Diabetic endothelial dysfunction: the role of poly(ADP - ribose) polymerase activation[J]. Nat Med,2001,7(1) :108- 113.

同被引文献46

  • 1张卫茹,侯凡凡,刘尚喜,郭志坚,周展眉,王国保,富宁,刘志强,王力,周玫.晚期糖基化终产物通过氧化应激加速动脉粥样硬化斑块形成[J].中华医学杂志,2004,84(13):1066-1070. 被引量:28
  • 2张隆,叶希韵,吕晔,李晓峰,王耀发.糖基化终产物和高糖对小牛主动脉血管细胞的损伤作用[J].基础医学与临床,2005,25(12):1161-1164. 被引量:2
  • 3Raingeaud J, Gupta S, Rogers JS, et al. Pro- inflammatory cytokines and environmental stress cause p38 mitogen activated protein kinase activation by dual phosphorylation on tyrosine and threonine[J]. J Biol Chem, 1995, 270(3): 7420-7426.
  • 4Lander HM. An essential role for free radicals and derived species in signal transduction[J]. FASEB J, 1997, 11(2):118- 124.
  • 5Wilhelm D, Bender K, Knebel A, et al. The level of intracellular glutathione is a key regulator for the induction of stress - activated signal transduction pathways including Jun N - terminal protein kinases and p38 kinase by alkylating agents[J].Mol Cell Biol, 1997, 17(8): 4792 - 4800.
  • 6Meister A. Glutathione deficiency produced by inhibition of its systhesis, and its reversal applications in research and therapy [J]. Pharmac Ther, 1991, 51(2): 155 - 194.
  • 7Finkel T, Holbrook NJ. Oxidants, oxidative stress and the biology of ageing[J]. Nature, 2000, 408(6809): 239- 247.
  • 8Droge W. Free radicals in the physiological control of cell function[ J]. Physiol Rev, 2002, 82(1): 47 - 95.
  • 9Thannickal V J, Fanburg BL. Reactive oxygen species in cell signaling[J]. Am J Physiol, 2000, 279(6): L1005 - L1028.
  • 10Finkel T. Redox- dependent signal transduction[J]. FEBS Lett, 2000, 476( 1 - 2): 52 - 54.

引证文献3

二级引证文献18

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部