ReviewCurrent opinion in genetics & development2014
Irreparable telomeric DNA damage and persistent DDR signalling as a shared causative mechanism of cellular senescence and ageing.
Review in Current opinion in genetics & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.
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
83 citing papers in PubMed, 155 citations in OpenAlex.
- Therapeutic inhibition of telomeric DNA damage response rescues hematopoietic dysfunction driven by telomere shortening and aging.Nature aging · 2026Article
- Transcriptomic analysis reveals a crucial role of the yolk sac during Avian Pathogenic Escherichia coli infection in chicken embryos.Poultry science · 2026Article
- Towards a context-aware framework for cellular senescence.Biogerontology · 2026Review
- Autophagy revealed as a targetable vulnerability in senescent cells by cell painting phenotypic profiling: a mechanistic study of MCOPPB and related compounds.GeroScience · 2026Article
- Senolytic reduction of senescent cells mitigates atrial arrhythmia vulnerability in aging rabbits.Heart rhythm · 2026Article
- CDK2 inhibitor BLU-222 synergizes with CDK4/6 inhibitors in drug resistant breast cancers through p21/p27 induction.Nature communications · 2026Article
- DsDNA breaks inflicted by cell-free chromatin particles selectively target telomeres.Scientific reports · 2025Article
- Prolonged exposure to leisure screen time notably accelerates biological aging: Evidence from observational studies and genetic associations.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Observational
- A transcriptome-based human universal senescence index (hUSI) robustly predicts cellular senescence under various conditions.Nature aging · 2025Article
- Carbon ion irradiation mobilizes antitumor immunity: from concept to the clinic.Radiation oncology (London, England) · 2025Review
- Ellagic acid alleviates PMToxicology research · 2025Article
- Prolonged Low-Dose Administration of FDA-Approved Drugs for Non-Cancer Conditions: A Review of Potential Targets in Cancer Cells.International journal of molecular sciences · 2025Review
- Centromere inactivation during aging can be rescued in human cells.Molecular cell · 2025Article
- Cellular Senescence in Health, Disease, and Lens Aging.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Studying Cellular Senescence Using the Model Organism Drosophila melanogaster.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Cellular senescence, neuroinflammation, and microRNAs: Possible interactions driving aging and neurodegeneration in the hippocampal neurogenic niche.Aging brain · 2025Review
- Senescence-like Phenotype After Chronic Exposure to Isoproterenol in Primary Quiescent Immune Cells.Biomolecules · 2024Article
- Alzheimer's Disease: Exploring the Landscape of Cognitive Decline.ACS chemical neuroscience · 2024Review
- Cumulative Dose from Recurrent CT Scans: Exploring the DNA Damage Response in Human Non-Transformed Cells.International journal of molecular sciences · 2024Article
- Cellular Aging and Senescence in Cancer: A Holistic Review of Cellular Fate Determinants.Aging and disease · 2024Review
23 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
The DNA damage response (DDR) orchestrates DNA repair and halts cell cycle. If damage is not resolved, cells can enter into an irreversible state of proliferative arrest called cellular senescence. Organismal ageing in mammals is associated with accumulation of markers of cellular senescence and DDR persistence at telomeres. Since the vast majority of the cells in mammals are non-proliferating, how do they age? Are telomeres involved? Also oncogene activation causes cellular senescence due to altered DNA replication and DDR activation in particular at the telomeres. Is there a common mechanism shared among apparently distinct types of cellular senescence? And what is the role of telomeric DNA damage?
Indexed as
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.