Objectives: The effects of therapeutic angiogenesis by intramuscular injection of early pro-angiogenic
cells (EPCs) into the ischemic limbs are unsatisfactory. The limb tissue may retain
the ischemia-induced oxidative stress and hence lead apoptosis of injected EPCs, resulting
in suboptimal clinical effects. It has been reported that Forkhead transcription factor
4 (FOXO4) plays a pivotal role in apoptosis signaling of EPCs in response to oxidative
stress. Accordingly, we assessed whether FOXO4-knockdown EPCs (FOXO4KD-EPCs) could suppress the oxidative stress-induced apoptosis and augment the neovascularization
capacity in ischemic limbs.
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EAS-0484
Identification
Copyright
© 2014 Published by Elsevier Inc.