Endothelial progenitor cell senescence--is there a role for estrogen?
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.
Imanishi
Toshio
T
Department of Cardiovascular Medicine, Wakayama Medical University, Wakayama, Japan. t-imani@wakayama-med.ac.jp
Tsujioka
Hiroto
H
Akasaka
Takashi
T
D000818:Animals; D016922:Cellular Senescence / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism; D004967:Estrogens / Q000378:metabolism / Q000494:pharmacology*; D006801:Humans; D007511:Ischemia / Q000378:metabolism / Q000503:physiopathology; D018919:Neovascularization, Physiologic; D017382:Reactive Oxygen Species / Q000378:metabolism; D013234:Stem Cells / Q000378:metabolism*; D019098:Telomerase / Q000378:metabolism
D004967:Estrogens; D017382:Reactive Oxygen Species; D019098:Telomerase