Skip to main content
. Author manuscript; available in PMC: 2019 Sep 1.
Published in final edited form as: Free Radic Biol Med. 2018 Mar 7;125:36–43. doi: 10.1016/j.freeradbiomed.2018.03.004

Figure 3. Impact of impaired redox signaling on DNA repair, telomere intactness and cellular aging.

Figure 3

ATM-dependent DNA repair pathways function optimally in a ROS rich environment. ROSlow RA T cells lack proper function of the kinase ATM and the nuclease MRE11A. Consequences include inappropriate repair of DNA double strand breaks and insufficient repair of telomeric ends. With persistent DNA damage responses and fragile telomeres, RA T cells enter the aging program prematurely. RA T cells express a typical aging signature, including p16hi, p21hi, CD57hi.