The role of reactive oxygen species in apoptosis of the diabetic kidney

被引：124

作者：

Wagener, F. A. D. T. G. ^{[1
]}

Dekker, D. ^{[1
]}

Berden, J. H. ^{[2
]}

Scharstuhl, A. ^{[1
]}

van der Vlag, J. ^{[2
]}

机构：

[1] Radboud Univ Nijmegen, Med Ctr, Dept Pharmacol & Toxicol, Nijmegen Ctr Mol Life Sci, NL-6500 HB Nijmegen, Netherlands

[2] Radboud Univ Nijmegen, Med Ctr, Nephrol Res Lab, Nijmegen Ctr Mol Life Sci,Dept Nephrol, NL-6500 HB Nijmegen, Netherlands

来源：

APOPTOSIS | 2009年 / 14卷 / 12期

关键词：

Diabetes; Apoptosis; Kidney; Diabetic nephropathy; Cytoprotective proteins; Anti-oxidants; TUBULAR EPITHELIAL-CELLS; INDUCED OXIDATIVE STRESS; HIGH AMBIENT GLUCOSE; HEME OXYGENASE-1; SUPEROXIDE ANION; TISSUE-INJURY; VITAMIN-C; EXPRESSION; HEPARANASE; DISEASE;

D O I：

10.1007/s10495-009-0359-1

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Increased levels of reactive oxygen species (ROS) by hyperglycemia can induce apoptosis of renal cells and diabetic nephropathy. The redox balance in the renal cell seems, therefore, of the utmost importance. ROS-mediated apoptosis may be further aggravated by an inadequate cytoprotective response against ROS. When there are insufficient cytoprotective and ROS scavenging molecules, ROS lead to considerable cellular damage and to a point of no return in apoptosis. Induction of cytoprotective proteins may prevent or attenuate apoptosis, renal cell injury, and finally diabetic nephropathy. Here, we discuss some mechanisms of apoptosis and several strategies that have been probed to ameliorate, or to prevent apoptosis in the diabetic kidney.

引用

页码：1451 / 1458

页数：8

共 73 条

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