Critical Role of the Nitric Oxide/Reactive Oxygen Species Balance in Endothelial Progenitor Dysfunction

被引:75
作者
Fleissner, Felix [1 ,2 ]
Thum, Thomas [1 ,2 ]
机构
[1] Hannover Med Sch, Inst Mol & Translat Therapeut Strategies, IFB Tx, Carl Neuberg Str 1, D-30625 Hannover, Germany
[2] Hannover Med Sch, Dept Cardiol & Angiol, D-30625 Hannover, Germany
关键词
SYNTHASE ENHANCER AVE9488; GROWTH-HORMONE TREATMENT; CORONARY-ARTERY-DISEASE; MARROW-DERIVED CELLS; OXIDE-SYNTHASE; OXIDATIVE STRESS; PERIPHERAL-BLOOD; MYOCARDIAL-INFARCTION; INDUCED MOBILIZATION; NEOINTIMA FORMATION;
D O I
10.1089/ars.2010.3502
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Endothelial injury and dysfunction are critical events in the pathogenesis of cardiovascular disease. During these processes, an impaired balance of nitric oxide bioavailability and oxidative stress is mechanistically involved. Circulating angiogenic cells (including early and late outgrowth endothelial progenitor cells (EPC)) contribute to formation of new blood vessels, neovascularization, and homeostasis of the vasculature, and are highly sensitive for misbalance between NO and oxidative stress. We here review the role of the endothelial nitric oxide synthase and oxidative stress producing enzyme systems in EPC during cardiovascular disease. We also focus on the underlying molecular mechanisms and potential emerging drug-and gene-based therapeutic strategies to improve EPC function in cardiovascular diseased patients. Antioxid. Redox Signal. 15, 933-948.
引用
收藏
页码:933 / 948
页数:16
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