RevieweLife2021
DNA damage-how and why we age?
Review in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 243 papers, 2 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
243 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- The impact of physical exercise on genotoxicity in older adults: a systematic review.Biogerontology · 2025Pooled it
- Broad repression of DNA repair genes in senescent cells identified by integration of transcriptomic data.Nucleic acids research · 2025Pooled it
- Energy constraint on human health.Trends in endocrinology and metabolism: TEM · 2026Review
- Proteostasis of organelles in aging and disease.The FEBS journal · 2026Review
- Skin Aging: From Molecular Mechanisms to Therapeutic and Technological Innovations.Journal of cellular and molecular medicine · 2026Review
- From cell to disease: Regulatory networks and mechanisms of super‑enhancers in aging (Review).Molecular medicine reports · 2026Review
- Article
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- Epigenetic remodeling during UV exposure: high resolution analysis of histone post-translational modifications in a DNA binding protein 2 mutant model.Histochemistry and cell biology · 2026Article
- MUTYH Cancer-Associated Variants Within the Interdomain Connector Differentially Impact Glycosylase Activity and Cellular DNA Repair.Chembiochem : a European journal of chemical biology · 2026Article
- Landscape of plastid DNA breaks in Arabidopsis during development and environmental stimulus.The Plant cell · 2026Article
- Review
- Psychosis as a multisystem disorder of aberrant aging.npj aging · 2026Review
- Facilitated DNA damage repair as an emerging therapeutic strategy for inflammatory and fibrotic diseases.RSC chemical biology · 2026Review
- Emerging role of radiopharmaceutical therapy in oncology: advances, challenges, and future directions.JNCI cancer spectrum · 2026Review
- Caloric restriction decelerates premature aging and cognitive decline in mice with deficient DNA repair.Communications biology · 2026Article
- Pleiotropy and disease interactors: the dual nature of genes linking ageing and ageing-related diseases.Biogerontology · 2026Article
- Stiffness-dependent alveolar type II cell senescence in idiopathic pulmonary fibrosis.Cell communication and signaling : CCS · 2026Article
- Biochemical Mechanisms of Cellular Stress Adaptation in the Pathogenesis of Chronic Diseases.Molecules (Basel, Switzerland) · 2026Review
- Age-associated increases in inter-individual gene expression variability across human tissues.bioRxiv : the preprint server for biology · 2026Article
183 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
6 authors.
Funding
Abstract
Aging is a complex process that results in loss of the ability to reattain homeostasis following stress, leading, thereby, to increased risk of morbidity and mortality. Many factors contribute to aging, such as the time-dependent accumulation of macromolecular damage, including DNA damage. The integrity of the nuclear genome is essential for cellular, tissue, and organismal health. DNA damage is a constant threat because nucleic acids are chemically unstable under physiological conditions and vulnerable to attack by endogenous and environmental factors. To combat this, all organisms possess highly conserved mechanisms to detect and repair DNA damage. Persistent DNA damage (genotoxic stress) triggers signaling cascades that drive cells into apoptosis or senescence to avoid replicating a damaged genome. The drawback is that these cancer avoidance mechanisms promote aging. Here, we review evidence that DNA damage plays a causal role in aging. We also provide evidence that genotoxic stress is linked to other cellular processes implicated as drivers of aging, including mitochondrial and metabolic dysfunction, altered proteostasis and inflammation. These links between damage to the genetic code and other pillars of aging support the notion that DNA damage could be the root of aging.
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.