评论文章
控制氧化还原状态对干细胞的生存,扩张,和分化
图2
由活性氧调控干细胞增殖和生存。(一)生理效应的ROS水平。生理水平的活性氧激活各种MAPKs(即。兵,p38和AKT),促进干细胞增殖。mir - 210是由活性氧和调节也参与MAPK的激活,导致增强的干细胞增殖。轻微的ROS水平促进pATM激活,增加干细胞的DNA稳定性。已经被轻微ROS能够维持抗菌性能和proangiogenic msc的函数。(b)的影响过多的活性氧水平。过度的ROS在干细胞诱导氧化应激水平。高浓度的活性氧导致干细胞粘附(即下降。, through a decreased activation of FAK-Src signaling) and proliferation (through the reduced activation of pRB). High ROS also reduce DNA stability and induce apoptosis (in favoring BAX-BAK dimerization and the formation of channel facilitating cytochrome c (cyt c) cytoplasmic translocation). In (a), Cyt c red means Cyt c reductase.
| (一) |
| (b) |