Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA 19140, USA.
Front Biosci (Landmark Ed). 2012 Jun 1;17(6):2327-49. doi: 10.2741/4055.
Endothelial progenitor cells (EPCs) are involved in the maintenance of endothelial homoeostasis and in the process of new vessel formation. Experimental and clinical studies have shown that atherosclerosis is associated with reduced numbers and dysfunction of EPCs; and that medications alone are able to partially reverse the impairment of EPCs in patients with atherosclerosis. Therefore, novel EPC-based therapies may provide enhancement in restoring EPCs' population and improvement of vascular function. Here, for a better understanding of the molecular mechanisms underlying EPC impairment in atherosclerosis, we provide a comprehensive overview on EPC characteristics, phenotypes, and the signaling pathways underlying EPC impairment in atherosclerosis.
内皮祖细胞（EPCs）参与内皮细胞的稳态维持和新血管形成过程。实验和临床研究表明，动脉粥样硬化与 EPCs 数量减少和功能障碍有关；而且药物单独作用就能部分逆转动脉粥样硬化患者 EPCs 的损伤。因此，基于 EPC 的新型治疗方法可能会增强恢复 EPC 数量和改善血管功能的效果。在这里，为了更好地理解动脉粥样硬化中 EPC 损伤的分子机制，我们全面概述了 EPC 的特征、表型以及动脉粥样硬化中 EPC 损伤的信号通路。
