ArticleNature communications2025
OGG1 and MUTYH repair activities promote telomeric 8-oxoguanine induced senescence in human fibroblasts.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- XRCC1 deficiency drives telomeric chromatin leakage, inflammatory signalling and senescence.Redox biology · 2026Article
- MUTYH Activity Maintains Telomere Stability in Response to Chronic Telomeric 8-Oxoguanine Damage in Cancer Cells.Biomolecules · 2026Article
- DENV-4 infection suppresses transcription of DNA repair genes.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- SMARCAL1 is a candidate therapeutic target for ALT-positive tumors.Genes & development · 2026Article
- An Integrated DNA Nanoprobe for Intranuclear Imaging and In Situ Profiling of OGG1 Activity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Facilitated DNA damage repair as an emerging therapeutic strategy for inflammatory and fibrotic diseases.RSC chemical biology · 2026Review
- Intermittent Fasting Enhances Genome Integrity and Cytoprotective Pathways via (BHB) β-Hydroxybutyrate Signaling and Chromatin Remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Epigenetic consequences of DNA damage.Molecular cell · 2026Review
- OGG1 and MUTYH DNA Glycosylases, the Dynamic Duo Against 8-Oxoguanine DNA Lesion: Structure, Regulation, and Novel Emerging Roles.Biomolecules · 2026Review
- [Chronic skin damage from UV radiation].Dermatologie (Heidelberg, Germany) · 2026Review
- Base excision repair within structure-forming repeat sequences and its impact on cancer and other diseases.NAR cancer · 2025Review
- Replication-associated base excision repair/single-strand break repair regulates PARG inhibitor response via the PRMT1/PRMT5/ATR axis.NAR cancer · 2025Article
- Telomeric DNA damage landscapes distinguish oxidative from inflammatory cellular stress.Nucleic acids research · 2025Article
- Article
- A steric gate prevents mutagenic dATP incorporation opposite 8-oxo-deoxyguanosine in mitochondrial DNA polymerases.The FEBS journal · 2025Article
- Oxidative Stress and DNA Damage at Telomeres.Cold Spring Harbor perspectives in biology · 2025Review
- Somatic mutations in angiogenesis-related pathways and RNA polymerase II activity in sporadic brain arteriovenous malformations.Frontiers in neurology · 2025Article
- BG4 antibody can recognize telomeric G-quadruplexes harboring destabilizing base modifications and lesions.Nucleic acids research · 2024Article
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Abstract
Telomeres are hypersensitive to the formation of the common oxidative lesion 8-oxoguanine (8oxoG), which impacts telomere stability and function. OGG1 and MUTYH glycosylases initiate base excision repair (BER) to remove 8oxoG or prevent mutation. Here, we show OGG1 loss or inhibition, or MUTYH loss, partially rescues telomeric 8oxoG-induced premature senescence and associated proinflammatory responses, while loss of both glycosylases causes a near complete rescue in human fibroblasts. Glycosylase deficiency also suppresses 8oxoG-induced telomere fragility and dysfunction, indicating that downstream single-stranded break (SSB) repair intermediates impair telomere replication. Preventing BER initiation suppresses PARylation and confers resistance to the synergistic effects of PARP inhibitors on 8oxoG-induced senescence. However, OGG1 activity is essential for preserving cell growth after chronic telomeric 8oxoG formation, whereas MUTYH promotes senescence to prevent chromosomal instability from unrepaired damage. Our studies reveal that inefficient completion of 8oxoG BER at telomeres triggers cellular senescence via SSB intermediates which disrupt telomere function.
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