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糖尿病肾病致足细胞损伤特点的研究 被引量：4

The Research on Characters of Podocytes Injury caused by Diabetic Nephropathy
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摘要 足细胞是附着在肾小球基底膜外的高度分化的上皮细胞,在维持肾小球滤过屏障完整性及限制血浆蛋白的滤出方面均发挥重要作用。近年来,在糖尿病肾病的研究中发现,足细胞损伤对蛋白尿及肾小球硬化等病理变化均明显相关。本文就糖尿病肾病时足细胞损伤的特点作一简要概述,为以后的相关研究奠定基础。 Podocyte is a kind of highly differentiated epithelial cells which attached to glomeroular basement meinbrance. Podocytes play a crucial role in preserving integrity of glomerular filtration barrier and maintaining specific restriction on filtration of plasma protein. In recent years, it was showed that the damage of podoeyte is related to proteinuria and glomerulosclerosis in the researching of diabetic nephropathy. This article reviews some papers in order to summarize the characters ofpodocytes injury caused by diabetic nephropathy and lay the foundation of correlational investigation.
作者 王万兴 王丽晔 郭思媛 李峰
机构地区 天津市武清区中医院 北京中医药大学
出处 《现代生物医学进展》 CAS 2012年第19期3774-3777,共4页 Progress in Modern Biomedicine
基金 国家自然科学基金面上项目(30873217) 国家自然科学青年基金项目(81001501) 国家质量工程中医特色建设项目(TS2067)
关键词 足细胞损伤 糖尿病肾病 特点 Podocyte injury Diabetic nephropathy Characters
分类号 R587.2 [医药卫生—内分泌]
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参考文献31

  • 1SaLmon AH, Neal CIL Harper SJ. New aspects of glomerular filtration barrier structuro and function: five layers (at least) not three [J]. Curr Opin Nephrol Hypertens,2009,18(3): 197-205.
  • 2Teiken JM, Audettey JL, Latumus DI, et al. Podocyte loss in aging OVE26 diabetic mice[J]. Anat Rec(Hoboken),2008,291 ( i ): 114-121.
  • 3Zanone MM, Favaro E, Doublier E. Expression of nephrin by human pancreatic islet endothelial cells [J]. Diabetologia, 2005, 48 (9): 1789-1797.
  • 4White KE, Bilous RW. Structural alterations to the podocyte are related to proteinuria in type 2 diabetic patients [J]. Nephrol Dial Transplant,2004,19(6): 1437-1440.
  • 5I Toyoda M, Najafian B, Kim Y, et al. Podoeyte detachment and reduced glomerular capillary endothelial fenestration in human type 1 diabetic nephropathy[J]. Diabetes,2007,56(8) :2155-2160.
  • 6Dalla VM, Masiero A, Roiter AM, et al. Is podocyte injury relevant in diabetic nephropathy studies in patients with type 2 diabetes [J]. 2003, 52(4): 1031-1035.
  • 7Dessapt C, Baradez MO, I-Iayward A, et al. Mechanical forces and TGFbetal reduce podoeyte adhesion through alpha3betal integrin downregulation [J]. Nephrol Dial Transolant,2009,24 (9):2645-2655.
  • 8Lemley KV. Diabetes and chronic kidney disease: Lessons from the Pima Indians [J]. Pediatr Nephrol,2008,23 (11):1933-1940.
  • 9Petermann AT, Krott R, Blonski M. et al. Podoeytes that detach in experimental membranous nephropathy are viable [J]. Kidney Int, 2003, 64(4): 1222-1231.
  • 10I Komai-Koma M, Jones L, Ogg GS, et al. TLR2 is expressed on activated T cells as a eostimulatory receptor [J]. Proe Natl Acad Sei USA, 2004, 101(9): 3029-3034.

二级参考文献39

  • 1Teiken JM, Audettey JL, Laturnus DI, et al. Podocyte loss in aging OVE26 diabetic mice [ J ]. Anat Rec (Hoboken), 2008, 291 (1): 114-121.
  • 2Salmon AH, Neal CR, Harper SJ. New aspects of glomerular filtration barrier structure and function: five layers (at least) not three [ J]. Curr Opin Nephrol Hypertens, 2009, 18 (3): 197-205.
  • 3Toyoda M, Najafian B, Kim Y, et al. Podocyte detachment and reduced glomerular capillary endothelial fenestration in human type 1 diabetic nephropathy [ J]. Diabetes, 2007, 56 (8): 2155-2160.
  • 4Wiggins JE, Goyal M, Sanden SK, et al. Podocyte hypertrophy, "adaptation" and " decompensation" associated with glomerular enlargement and glomerulosclerosis in the aging rat : prevention by calorie restriction [J]. J Am Soc Nephrol, 2005, 16 (10): 2953- 2966.
  • 5Dessapt C, Baradez MO, Hayward A, et al. Mechanical forces and TGFbetal reduce podocyte adhesion through alpha3beta1 integrin downregulation [ J ]. Nephrol Dial Transplant, 2009, 24 (9): 2645 - 2655.
  • 6Lemley KV. Diabetes and chronic kidney disease: Lessons from the Pima Indians [ J ]. Pediatr Nephrol, 2008, 23 (11): 1933-1940.
  • 7Ruster C, Bondeva T, Franke S, et al. Advanced glycation end - products induce cell cycle arrest and hypertrophy in podocytes [ J ]. Nephrol Dial Transplant, 2008, 23 (7): 2179-2191.
  • 8Harita Y, Kurihara H, Kosako H, et al. Phosphoryla- tion of nephrin triggers Ca^2+ signaling by recruitment and activation of phospholipase C - { gamma} 1 [ J]. J Biol Chem, 2009, 284 (13): 8951-8962.
  • 9Menne J, Meier M, Park JK, et al. Nephrin loss in experimental diabetic nephropathy is prevented by deletion of protein kinase C alpha signaling in - vivo [ J ]. Kidney Int, 2006, 70 (8) : 1456 - 1462.
  • 10Forbes JM, Bonnet F, Russo LM, et al. Modulation of nephrin in the diabetic kidney: association with systemic hypertension and increasing albuminuria [ J]. J Hypertens, 2002, 20 (5): 985-992.

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二级引证文献7

现代生物医学进展
2012年 第19期

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