Key result
Estrogen reduces endothelial progenitor cell senescence through augmentation of telomerase activity, potentially improving functional activity for cell therapy.
Why the study?
Does estrogen prevent endothelial progenitor cell senescence?
Does estrogen prevent endothelial progenitor cell senescence?
Estrogen may play a beneficial role in preventing endothelial progenitor cell senescence and improving their functional activity for ischemic tissue repair.
Hypothesis-generating for estrogen-enhanced EPC therapy in ischemia; leaves open clinical translation and safety.
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.
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Imanishi et al. (2009) conducted a review in Endothelial progenitor cell senescence. Estrogen was evaluated. Estrogen reduces endothelial progenitor cell senescence through augmentation of telomerase activity, potentially improving functional activity for cell therapy.
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