Fig. 7: Model for telomere 8oxoG induced senescence.
From: Telomeric 8-oxo-guanine drives rapid premature senescence in the absence of telomere shortening
Following induction of ROS by endogenous or exogenous stressors, telomeres are susceptible to oxidative DNA damage, including formation of the common lesion 8oxoG. When a replication fork encounters 8oxoG in the telomere, it may stall, resulting in excess ssDNA, leading to replication stress. Replication stress can lead to telomere fragility, localized DDR signaling and MiDAS repair at the telomere. Telomere DDR results in p53 activation, which promotes cellular senescence including multiple characteristic hallmarks. Imagine created with BioRender.com.
