Endothelial progenitor cell dysfunction in type I diabetes: Another consequence of oxidative stress?

被引:57
|
作者
Loomans, CJM
De Koning, EJP
Staal, FJT
Rabelink, TJ
Van Zonneveld, AJ
机构
[1] Leiden Univ, Med Ctr, Dept Nephrol, NL-2333 ZA Leiden, Netherlands
[2] Erasmus MC, Dept Immunol, Rotterdam, Netherlands
关键词
D O I
10.1089/ars.2005.7.1468
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
Endothelial progenitor cells (EPC) have been shown to contribute to neovascularization and vascular maintenance and repair in adults. Recently, the concept has evolved that EPC dysfunction, in patients at risk for cardiovascular disease, may contribute to the development of atherosclerosis and ischemic vascular disease. Particularly, patients with diabetes mellitus are likely to be affected by EPC dysfunction as several studies have shown a reduced number and function of EPC in patients, as well as in preclinical models for type 1 diabetes. Here, we review our current understanding of EPC (dys)function in diabetes and discuss some potential mechanisms underlying their altered properties. Moreover, we provide circumstantial evidence indicating that increased oxidative stress could play a role in the development of EPC dysfunction in type 1 diabetes. Finally, we discuss the potential implication of our findings for EPC-based therapies and the potential impact of pharmacological interventions on the vascular regenerative capacity of EPC.
引用
收藏
页码:1468 / 1475
页数:8
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