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信号转导通路与糖尿病肾病的关系 被引量:1

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摘要 糖尿病是胰岛素分泌缺陷和(或)胰岛素作用障碍而导致的一组以高血糖为特征的慢性代谢性疾病。长期高血糖状态可以导致包括肾脏在内的多种组织器官的损伤和功能障碍。随着人民生活水平的不断提高,糖尿病发病率逐年上升。目前全球约有1.5亿糖尿病患者。我国约有3000万名糖尿病患者,而糖尿病的各种慢性并发症已成为糖尿病致残致死的主要病因。作为慢性并发症之一的糖尿病。肾病(DN)是糖尿病致残因素和重要的死亡原因之一。
作者 吴英 王力宁
出处 《临床内科杂志》 CAS 2010年第3期212-214,共3页 Journal of Clinical Internal Medicine
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参考文献18

  • 1王金泉,刘志红.终末期糖尿病肾病肾替代治疗[J].医学研究生学报,2006,19(7):664-668. 被引量:20
  • 2Wendt T,Tanji N,Guo J,et al.Glucose,glycation and RAGE:implications for amplification of cellular dysfunction in diabetic nephropathy.J AM Soc Nephrol,2003,14:1383-1395.
  • 3Linden KC,De Haan CL,Zhang Y,et al.Renal expression and Localezation of the facilitative glucose transporters GLVT1 and GLVTI 2 in animal models of hy Rentention and diabetic nephropathy.Am J Physiol Renal Physiol,2006,290:F205-213.
  • 4Zintzaras E,Stefamidis I.Association between the GLUT1 gene polymorphism and the risk of diabetic nephropathy:a meta-analysis.J Hum Genet,2005,50:84-91.
  • 5Yanagishi S,Fukemi K,Ueda S,et al.Molecuar mechanisms of diabetic nephropathy and its therapeutic intervention.Curt Drug Targets,2007,8:952-959.
  • 6FomoniA,IjezA,Tejeda T,et al.Role of infemmation in diabetic nephropathy.Curr Diabetics,2008,4:10-17.
  • 7GiuntiS,Tesch GH,Pinach S,et al.Monocyte ehemoattractantprotein-1 has prosclerotic effects both in a mouse model uf experimental diabetea and in vitro in human mesangial cells.Diabetobgia,2008,51:198-207.
  • 8Lane P.Diabetic kidney disease:impact of puberty.Am J physiol Renal Physiol,2002,283:F589-600.
  • 9Ha H,Yu MR,Choi YJ,et al.Role of high glucose-induced nuclear factot KB activation in monocyte chemoattractant proteirr-1 expression by mesangial cells.J Am Soc,Nephrol,2002,13:894-902.
  • 10Ha H,Yang Y,Lee HB.Mechanisms of reactive oxygen species generation in LLC-PK1 Cells Cultured under high glucose.J Am Soc Nephrol,2002.13:531-534.

二级参考文献46

  • 1彭毅,龚小卫,姜勇.肌动蛋白相关蛋白2/3复合体的结构、功能与调节[J].生理科学进展,2004,35(4):306-310. 被引量:8
  • 2王谦,肖争流,胡斌,李长贵.醛糖还原酶基因多态性与糖尿病肾病的相关性研究[J].医学研究生学报,2005,18(4):346-348. 被引量:2
  • 3Yang J, Liu Y. Dissection of key events in tubular epithelial to myofibroblast transition and its implications in renal interstitial fibrosis. Am J Pathol, 2001,159:1465-1475.
  • 4Yang J, Liu Y. Blockage of tubular epithelial to myofibroblast transition by hepatocyte growth factor prevents renal interstitial fibrosis. J Am Soc Nephrol, 2002,13:96-107.
  • 5Iwano M, Plieth D, Danoff TM, et al. Evidence that fibroblasts derive from epithelium during tissue fibrosis. J Clin Invest, 2002,110:341-350.
  • 6Yang J, Shuhz RW, Mars WM, et al. Disruption of tissuetype plasminogen activator gene in mice reduces renal interstitial fibrosis in obstructive nephropathy. J Clin Invest, 2002,110:1525-1538.
  • 7Gorg A, Weiss W, Dunn MJ. Current two-dimensional eleetrophoresis technology for proteomies. Proteomies, 2004, 4: 3665 - 3685.
  • 8Lan HY. Tubular epithelial-myofibroblast transdifferentiation mechanisms in proximal tubular cells. Curt Opin Nephrol Hypertens, 2003,12:25-29.
  • 9Lan HY, Mu W, Tomita N, et al. Inhibition of renal fibrosis by gene transfer of inducible Smad7 using ultrasoundmicrobubble system in rat UUO model. J Am Soc Nephrol, 2003,14:1535-1548.
  • 10Zeidan A, Sward K, Nordstrom I, et al. Ablation of SM22alpha decreases contractility and actin contents of mouse vascular smooth muscle. FEBS Lett, 2004,562:141- 146.

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  • 1JE Toblli,Monica G,F Gabriel,et al. Antifibrotic effects of piogl itazone on the kidney in a rat model of type 2 diabetes mellitus [J]. Nephrol Dial Transplant.2009,2.1(8):2349.
  • 2Katavetin P, Eiam-Ong S. Suwanwalaikorn S. Pioglitazone re duces urinary protein and urinary transforming growth factor be ta excretion in patients with type 2 diabetes and overt nephrnpa thy[J]. J Med Assoc Thai,2006,89(2):170.
  • 3Yang J,Zhang D,I.i J,et al. Role of PPAR r in renoprmection in Type 2 diabetes, molecularmeehanisms and therapeutic polential [J]. Clin Sci,2009,116(1) : 17.
  • 4SY Han,CH Kim, HS Kim, et al, Spironolactone prevents diabel- ie nephropathy through an anti-inflammatory mechanism in type 2 diabetic rats[J]. J Am Soe Nephrol,2006.17(5) : 1362.
  • 5Wada T, Furuichi K. Sakai N, el al. Up-regulation of monocyte chemoattractam protein-1 in tubulointerstitial lesions of human diabetic nephropathy[J]. Kidney Int, 2000,58( 1 ) : 1492.
  • 6Kanwar YS,Wada J, Sun I., et al. Diabetic nephopathy: mecha nisms of renal diaease progression[J]. Exp Biol Med. 2008, 223 (1):4.
  • 7Oalkina E,et al. Leukocyte recruitment and vascuIar injury in dia betic nephropathy[J]. J Am Soe Nephrol,2006.17(2) :368.
  • 8Ruster C. wolf G. The role of ehemokines and chmokine recep- tors in diabetic nephropathy[J]. Front Biosci, 2008,13 : 941.
  • 9Tesch HG. MCP I/CCL L2:a new diagnostic marker and thera peulic targel for progressive renal injury in diabetic nephropathy [J]. Am J Physiol Renal Physiol. 2008.29/( 1 ) : 697.
  • 10Ha H,Yu MR.Choi YJ,et al. Role of high glucose induced nu clear factor-kappa B actiwllion in monocyle eherlloattraielant protein-1 expression by mesangial cells[J]. J Am Soc Nephrol, 2002,13(4) :894.

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