期刊文献+

炎性反应在糖尿病视网膜病变中的作用 被引量:1

原文传递
导出
摘要 糖尿病视网膜病变是最常见、最重要的糖尿病微血管并发症之一,是主要的致盲性眼病。研究表明,炎性反应及细胞因子导致视网膜微血管损伤,血一视网膜屏障破坏,视网膜缺血和代谢障碍,视网膜神经元凋亡,在糖尿病视网膜病变的发生、发展中起了十分重要的作用。在整个病变过程中细胞因子是反映炎性反应和病变严重程度的敏感指标。交感神经损伤可导致炎性反应发生,促进糖尿病视网膜病变的发生。
出处 《国际眼科纵览》 2011年第3期165-167,共3页 International Review of Ophthalmology
  • 相关文献

参考文献27

  • 1Defraigne JO. A central pathological mechanism explaining diabetic complications. Rev Med Liege, 2005, 60: 472-478. 被引量:1
  • 2Takenaka K, Yamagishi S, Matsui T, et al. Role of advanced gly- cation end products (AGEs) in thrombogenic abnormalities in dia- betes. Curr Neurovasc Res, 2006, 3 : 73-77. 被引量:1
  • 3Augustin AJ. Oxidative tissue damage. Klin Monbl Augenheilkd, 2010, 227 : 90-98. 被引量:1
  • 4Steinle JJ. Sympathetic nerves regulate inflammatory markers in the rat retina. Invest Ophthalmol Vis Sci, 2006, 47: 1735. 被引量:1
  • 5Meleth A, Agr6n E, Chan CC, et al. Serum inflammatory markers in diabetic retinopathy. Invest Ophthalmol Vis Sci, 2005, 46: 4295 -4301. 被引量:1
  • 6Miyamoto K, Khosrof S, Bursell SE, et al. Prevention of leukostasis and vascular leakage in streptozotocin induced diabetic retinopathy via intercellular adhesion molecule-1 inhibition. Proc Natl Acad Sci USA, 1999, 96 : 10836-10841. 被引量:1
  • 7哈文静,严宏.炎症在糖尿病视网膜病变发病机制中的作用[J].国际眼科杂志,2005,5(4):745-749. 被引量:15
  • 8Harris AG, Skalak TC, Hatchell DL. Leukocyte-capillary plugging and network resistance are increased in skeletal muscle of rats with streptozotocin-induced hyperglycemia. Int J Microcirc, 1994, 14 : 159-166. 被引量:1
  • 9Joussen AM, Murata T, Tsujikawa A, et al. Leukocyte-mediated endothelial cell injury and death in the diabetic retina. Am J Pathol, 2001, 158: 147-152. 被引量:1
  • 10Zheng L, Szabo C, Kern TS. Poly (ADP-ribose) polymerase is involved in the development of diabetic retinopathy via regulation of nuclear faetor-KB. Diabetes, 2004, 53: 2960-2967. 被引量:1

二级参考文献40

  • 1哈文静,严宏.炎症在糖尿病视网膜病变发病机制中的作用[J].国际眼科杂志,2005,5(4):745-749. 被引量:15
  • 2Qaum T,Xu Q,Joussen AM,Clemens MW,Qin W,Miyamoto K,Hassessian H,Wiegand SJ,Rudge J,Yancopoulos GD,Adamis AP.VEGF-initiated blood-retinal barrier breakdown in early diabetes.Invest Ophthalmol Vis Sci,2001;42(10):2408-2413. 被引量:1
  • 3Lu M,Perez VL,Ma N,Miyamoto K,Peng HB,Liao JK,Adamis AP.VEGF increases retinal vascular ICAM-1 expression in vivo.Invest Ophthalmol Vis Sci,1999;40(8):1808-1812. 被引量:1
  • 4Miyamoto K,Khosrof S,Bursell SE,Moromizato Y,Aiello LP,Ogura Y,Adamis AP.Vascular endothelial growth factor(VEGF)-induced retinal vascular permeability is mediated by intercellular adhesion molecule-1(Ⅰ-CAM-1).Am J Pathol,2000;156(5):1733-1739. 被引量:1
  • 5Aiello LP,Bursell SE,Clermont A,Duh E,Ishii H,Takagi C,Mori F,Ciulla TA,Ways K,Jirousek M,Smith LE,King GL.Vascular endothelial growth factor-induced retinal permeability is mediated by protein kinase Cin vivo and suppressed by an orally effective beta-isoform-selective inhibitor.Diabetes,1997;46(9):1473-1480. 被引量:1
  • 6Ishida S,Usui T,Yamashiro K,Kaji Y,Ahmed E,Carrasquillo KG,Amano S,Hida T,Oguchi Y,Adamis AP.VEGF164 is proinflammatory in the diabetic retina.Invest Ophthalmol Vis Sci,2003;44(5):2155-2162. 被引量:1
  • 7Peppa M,Uribarri J,Vlassara H.Glucose,advanced glycation end products,and diabetes complications:what is new and what works.Clin Diabetes,2003;21(4):186-187. 被引量:1
  • 8Basta G,Schmidt AM,De Caterina R.Advanced glycation end products and vascular inflammation:implications for accelerated atherosclerosis in diabetes.Cardiovasc Res,2004;63(4):582-592. 被引量:1
  • 9Hori O,Yan SD,Ogava S,Kuwabara K,Matsumoto M,Stern D,Schmidt AM.The receptor for advanced glycation end-products has a central role in mediating the effects of advanced glycation end-products on the development of vascular disease in diabetes mellitus.Nephrol Dial Transplant,1996;(11)5:13-16. 被引量:1
  • 10Basta G,Lazzerini G,Massaro M,Simoncini T,Tanganelli P,Fu C,Kislinger T,Stern DM,Schmidt AM,De Caterina R.Advanced glycation end products activate endothelium through signal-transduction receptor RAGE:a mechanism for amplification of inflammatory responses.Circulation ,2002;105(7):816-822. 被引量:1

共引文献14

同被引文献20

引证文献1

二级引证文献2

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