Imanishi Toshio, Tsujioka Hiroto, Akasaka Takashi
Department of Cardiovascular Medicine, Wakayama Medical University, Wakayama, Japan.
Ther Adv Cardiovasc Dis. 2010 Feb;4(1):55-69. doi: 10.1177/1753944709353173. Epub 2009 Dec 4.
Recent studies have demonstrated that aging or senescence constitutes a potential limitation to the ability of endothelial progenitor cells (EPCs) to sustain ischemic tissue repair. Excess amount of reactive oxygen species (ROS) is involved in senescence, causing defective neovascularization. Conversely, estrogens have been shown to accelerate recovery of the endothelium after vascular injury. Estrogen reduces EPC senescence through augmentation of telomerase activity. In addition, the inhibition of EPC senescence by estrogen in vitro may improve the functional activity of EPCs in a way that is important for potential cell therapy. This review describes current understanding of EPC senescence and the role of estrogen in preventing EPC senescence.
最近的研究表明，衰老构成了内皮祖细胞（EPCs）维持缺血组织修复能力的潜在限制。过量的活性氧（ROS）参与衰老过程，导致新生血管形成缺陷。相反，雌激素已被证明可加速血管损伤后内皮的恢复。雌激素通过增强端粒酶活性来减少EPC衰老。此外，雌激素在体外对EPC衰老的抑制作用可能以一种对潜在细胞治疗很重要的方式改善EPC的功能活性。本综述描述了目前对EPC衰老的认识以及雌激素在预防EPC衰老中的作用。
