ArticleNature cell biology2012
Telomeric DNA damage is irreparable and causes persistent DNA-damage-response activation.
Article in Nature cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 466 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
466 citing papers in PubMed, 3 syntheses or guidelines pooled it, 815 citations in OpenAlex.
- Protective Effects of Micronutrient Supplements, Phytochemicals and Phytochemical-Rich Beverages and Foods Against DNA Damage in Humans: A Systematic Review of Randomized Controlled Trials and Prospective Studies.Advances in nutrition (Bethesda, Md.) · 2023Pooled it
- Disrupting Mechanisms that Regulate Genomic Repeat Elements to Combat Cancer and Drug Resistance.Frontiers in cell and developmental biology · 2022Pooled it
- Chronological Age Affects MSC Senescence In Vitro-A Systematic Review.International journal of molecular sciences · 2021Pooled it
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- Effects of Telomere Related Senescence-Genes in Cervical Cancer.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Replicative and Air Pollution-Induced Senescence: Telomere Dysfunction, Mitochondrial Stress, and Modulatory Effects of Astragaloside IV in Endothelial and Vascular Smooth Muscle Cells.Cardiovascular toxicology · 2026Article
- The telomeric DNA damage response as a therapeutic target in idiopathic pulmonary fibrosis.EMBO molecular medicine · 2026Article
- Timing-Dependent Clearance of p16-Positive Cells Mitigates Radiation-Induced Accelerated Aging.Aging cell · 2026Article
- TRF2 enriched cytoplasmic chromatin drives cGAS-STAT1-mediated inflammation in senescence.iScience · 2026Article
- Review
- Diverse Forms of Autophagy and Their Roles in Liver Disease and Aging: A Comprehensive Review.Proteomes · 2026Review
- Article
- Research progress on cellular senescence in the pathogenesis and treatment of osteoarthritis and temporomandibular joint osteoarthritis.Journal of oral & facial pain and headache · 2026Review
- Telomere Dysfunction and Proteostasis Decline Define Distinct Pathways of Cellular Senescence in the Human Respiratory Tract.Aging cell · 2026Article
- Exceptional Longevity Modifying Allele APOE2 Promotes DNA Signaling Pathways Resisting Cellular Senescence in Human Neurons.Aging cell · 2026Article
- Review
- Molecular evolution of animal aging.The EMBO journal · 2026Review
- Senolytic reduction of senescent cells mitigates atrial arrhythmia vulnerability in aging rabbits.Heart rhythm · 2026Article
- Replicative senescence induction in single cells is not predicted by telomere length, dysfunction, or oxidation.iScience · 2026Article
- G1/S arrest: a key mechanism of cellular aging and replicative senescence.Biogerontology · 2026Review
406 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
- Erratum issued
Authors and funding
13 authors at 6 institutions in 3 countries.
Funding
Abstract
The DNA-damage response (DDR) arrests cell-cycle progression until damage is removed. DNA-damage-induced cellular senescence is associated with persistent DDR. The molecular bases that distinguish transient from persistent DDR are unknown. Here we show that a large fraction of exogenously induced persistent DDR markers is associated with telomeric DNA in cultured cells and mammalian tissues. In yeast, a chromosomal DNA double-strand break next to a telomeric sequence resists repair and impairs DNA ligase 4 recruitment. In mammalian cells, ectopic localization of telomeric factor TRF2 next to a double-strand break induces persistent DNA damage and DDR. Linear, but not circular, telomeric DNA or scrambled DNA induces a prolonged checkpoint in normal cells. In terminally differentiated tissues of old primates, DDR markers accumulate at telomeres that are not critically short. We propose that linear genomes are not uniformly reparable and that telomeric DNA tracts, if damaged, are irreparable and trigger persistent DDR and cellular senescence.
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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.