Endothelial progenitor cells in cardiovascular disease and hypoxia-potential implications to obstructive sleep apnea

被引:36
作者
Berger, Slava [1 ]
Lavie, Lena [1 ]
机构
[1] Technion Israel Inst Technol, Bruce & Ruth Rappaport Fac Med, Unit Anat & Cell Biol, Lloyd Rigler Sleep Apnea Res Lab, IL-31096 Haifa, Israel
关键词
MESENCHYMAL STEM-CELLS; ISCHEMIC PRECONDITIONING PROTECTS; ACUTE MYOCARDIAL-INFARCTION; NITRIC-OXIDE SYNTHASE; FACTOR-KAPPA-B; OXIDATIVE STRESS; INTERMITTENT HYPOXIA; PLASMA-LEVELS; DEPENDENT VASODILATION; CLINICAL-IMPLICATIONS;
D O I
10.1016/j.trsl.2010.12.008
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
100118 [医学信息学]; 100208 [临床检验诊断学];
摘要
In recent years, endothelial progenitor cells (EPCs) have gained a central role in vascular regeneration and endothelial repair capacity through angiogenesis and restoring endothelial function of injured blood vessels. These bone-marrow-derived cells are capable of promoting neovascularization, improving blood perfusion, and facilitating the recovery of ischemic tissues through differentiation into functional endothelial cells and secretion of angiogenic mediators. Obstructive sleep apnea (OSA) syndrome is characterized by recurrent episodes of intermittent hypoxia (IH), which can lead to endothelial dysfunction, atherosclerosis, as well as cardiovascular morbidity and mortality. However, IH also may contribute to cardioprotection and the development of collateral vessels by mobilizing progenitor cells to the circulation and damaged myocardium. Accumulating evidence in recent years suggests that EPCs are decreased in patients with endothelial dysfunction and underlie an increased risk for cardiovascular morbidity in OSA. The current review highlights the potential role of EPCs in the pathogenesis of vascular diseases that is pertinent to OSA. (Translational Research 2011;158:1-13)
引用
收藏
页码:1 / 13
页数:13
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