ArticleRedox biology2018
Spontaneous DNA damage to the nuclear genome promotes senescence, redox imbalance and aging.
Article in Redox biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
What it found
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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
81 citing papers in PubMed.
- Energy constraint on human health.Trends in endocrinology and metabolism: TEM · 2026Review
- Article
- Fueling the fire: metabolic dysfunction and senescence as drivers of lung aging and disease.Physiological reviews · 2026Review
- Review
- Immunosenescence in Idiopathic Pulmonary Fibrosis.Journal of inflammation research · 2026Review
- Genomic structural equation modeling decodes skeletal aging: novel loci discovery and multisystem genetic crosstalk.Journal of translational medicine · 2025Article
- Low-Dose radiation risk in medicine: a look at risk models, challenges, and future prospects.Zeitschrift fur medizinische Physik · 2025Review
- The context-dependent effect of cellular senescence: From embryogenesis and wound healing to aging.Ageing research reviews · 2025Review
- Attenuation of Cellular Senescence and Improvement of Osteogenic Differentiation Capacity of Human Liver Stem Cells Using Specific Senomorphic and Senolytic Agents.Stem cell reviews and reports · 2025Article
- Review
- Redox regulation: mechanisms, biology and therapeutic targets in diseases.Signal transduction and targeted therapy · 2025Review
- Trends of genetic contributions on epigenetic clocks and related methylation sites with aging: A population-based adult twin study.Aging cell · 2025Article
- The Ercc1Aging cell · 2025Article
- Multidimensional mechanisms of quercetin in diabetic kidney disease.Frontiers in cell and developmental biology · 2025Review
- Beyond polarization: macrophage senescence in immunoregulation and cancer therapy.International journal of biological sciences · 2025Review
- Transcriptional stress in aging: integrating experimental data and modeling to quantify DNA damage accumulation.Frontiers in molecular biosciences · 2025Article
- Beyond Nucleotide Excision Repair: The Importance of XPF in Base Excision Repair and Its Impact on Cancer, Inflammation, and Aging.International journal of molecular sciences · 2024Review
- Review
- The brain-body energy conservation model of aging.Nature aging · 2024Review
- Senescence- and Immunity-Related Changes in the Central Nervous System: A Comprehensive Review.Aging and disease · 2024Review
21 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
42 authors.
Funding
Abstract
Accumulation of senescent cells over time contributes to aging and age-related diseases. However, what drives senescence in vivo is not clear. Here we used a genetic approach to determine if spontaneous nuclear DNA damage is sufficient to initiate senescence in mammals. Ercc1
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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.