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. 2022 Jun 30;29(7):639–652. doi: 10.1038/s41594-022-00790-y

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — 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.