ReviewNature reviews. Drug discovery2025
Targeting DNA damage in ageing: towards supercharging DNA repair.
Review in Nature reviews. Drug discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis 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
17 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Antioxidant enzymes, oxidative stress, and physiological aging markers in Drosophila melanogaster (Diptera: Drosophilidae): a systematic review with translational perspectives.Journal of insect science (Online) · 2026Pooled it
- Could mending damaged DNA prolong life?Nature · 2026Article
- Reprogramming the Immunosuppressive Microenvironment in Triple-Negative Breast Cancer via FAP-Targeted Nanoprobes for Multimodal Imaging and Photothermal Therapy.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Mitochondrial protein COXFA4L3 (C15ORF48) confers resistance to DNA-damaging anticancer agents by repressing mitochondrial DNA damage responses.Scientific reports · 2026Article
- Facilitated DNA damage repair as an emerging therapeutic strategy for inflammatory and fibrotic diseases.RSC chemical biology · 2026Review
- Comparative whole-genome analyses of articular chondrocytes and skin fibroblasts reveal distinct genome instability landscapes in mesenchymal cell types.PLoS genetics · 2026Article
- Nanotechnology-driven STING regulation for on-demand therapy.Acta pharmaceutica Sinica. B · 2026Review
- DNA Damage Across Dietary Patterns: A Comet Assay Study in Vegans and Omnivores.Foods (Basel, Switzerland) · 2026Article
- Biochemical Mechanisms of Cellular Stress Adaptation in the Pathogenesis of Chronic Diseases.Molecules (Basel, Switzerland) · 2026Review
- Subtle-seq reveals frequent ageing-associated chromosome fragmentation on nucleosome core DNA.Nucleic acids research · 2026Article
- Molecular evolution of animal aging.The EMBO journal · 2026Review
- Insights into Tardigrade Damage-Suppression Protein, Dsup.Biomolecules · 2026Review
- Comparative whole-genome analyses of articular chondrocytes and skin fibroblasts reveal distinct genome instability landscapes in mesenchymal cell types.bioRxiv : the preprint server for biology · 2026Article
- Integrated multi-omics profiling identifies aging-related molecular signatures and convergent interferon signaling in systemic lupus erythematosus.Frontiers in immunology · 2026Article
- A pan-cancer analysis of the oncogenic role of KIF13A in human tumors.Discover oncology · 2025Article
- Article
- Epigenetic pharmacology in aging: from mechanisms to therapies for age-related disorders.Frontiers in pharmacology · 2025Review
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.
Funding
Abstract
Ageing is the most important risk factor for many common human diseases, including cancer, diabetes, neurodegeneration and cardiovascular disease. Consequently, combating ageing itself has emerged as a rational strategy for addressing age-related multimorbidity. Over the past three decades, multiple genetic and pharmacologic interventions have led to substantial extension of lifespan and healthspan in model organisms. However, it is unclear whether these interventions target the causal mechanisms of ageing or downstream consequences. Ample evidence suggests that DNA damage to the somatic genome is a major causal mechanism of ageing, which compromises essential cellular functions such as transcription and replication, and leads to cellular senescence, apoptosis and mutations. Recently, new concepts have emerged to target the main consequences of DNA damage and enhance DNA repair capacities, thereby extending maintenance of the genome. Here, we review advances in this field and discuss approaches to pharmacologically mitigate the adverse effects of DNA damage to delay ageing, prevent mutation-driven cancer and mitigate age-related degenerative diseases.
Indexed as
Identifiers
What Socratic 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 Socratic graph.