基础医学与临床 ›› 2012, Vol. 32 ›› Issue (11): 1360-1363.

• 短篇综述 • 上一篇    下一篇

糖代谢紊乱致肾小球内皮细胞损伤机制进展

王臻,陆利民   

  1. 复旦大学上海医学院生理与病理生理系
  • 收稿日期:2011-08-26 修回日期:2012-03-28 出版日期:2012-11-05 发布日期:2012-10-19
  • 通讯作者: 陆利民 E-mail:lulimin@shmu.edu.cn

Progress in high glucose-induce glomerular endothelial cells injury in diabetic nephropathy

  • Received:2011-08-26 Revised:2012-03-28 Online:2012-11-05 Published:2012-10-19

摘要: 糖尿病肾病是糖尿病的重要慢性并发症之一,高糖状态下肾脏小球内皮细胞的损伤与糖尿病肾病的发生、发展有密切的联系。高糖可以导致肾脏的多种活性物质,包括血管紧张素Ⅱ(Ang II)、内皮生长因子(VEGF)、活性氧(ROS)、糖基化终末产物(AGEs)等发生改变,而这些变化都可引起内皮细胞的功能障碍,进一步参与糖尿病肾脏损害的发生和发展。

关键词: 内皮细胞, 血管内皮功能障碍, 糖尿病, 肾病

Abstract: Diabetic nephropathy is one of the most important complications of diabetes. The exactly molecular mechanism underlines that the abnormality in glucose metabolism leads to renal damages is still not completely revealed. However, it has been noticed that the renal vascular endothelial dysfunction is involved in the incidence and plays an important role in development of diabetic nephropathy. Angiotensin II (Ang II), vascular endothelial growth factor (VEGF), reactive oxygen species (ROS), advanced glycocylation end products (AGEs) are all demonstrated contribute to hyperglycemia induced renal endothelial dysfunction. In this review, we summarized the recent evidences in hyperglycemia induced renal vascular endothelial dysfunction, and development of diabetic nephropathy.

Key words: Endothelium, Vascular endothelial dysfunction, Diabetes, Nephropathy

中图分类号: