ReviewBlood2018
DNA damage responses and p53 in the aging process.
Review in Blood, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 215 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
215 citing papers in PubMed, 386 citations in OpenAlex.
- Herbal Formula AC591 Protects Against Cisplatin-Induced Hearing Loss by Inhibiting p53-Mediated Ferroptosis.Smart medicine · 2026Article
- FUNDC1 Attenuates UVA-Induced Skin Photoaging by Regulating Mitophagy and P53 Stability.Antioxidants (Basel, Switzerland) · 2026Article
- Hepatic Cellular Senescence Is Attenuated by Filbertone via Modulation of the p53-p21 Pathway in AML12 Hepatocytes.Nutrients · 2026Article
- Identification of MKRN1 as a key modulator of the p53-MDM2 feedback loop.Cell death and differentiation · 2026Article
- Staphylococcus aureus rewires arginine metabolism to drive mammary aging via macrophage-epithelial crosstalk.PLoS pathogens · 2026Article
- Combination of Ophiopogonin D, Ginsenoside Rg1, and Ginsenoside Rg3 ameliorates idiopathic pulmonary fibrosis via inhibiting type 2 alveolar epithelial cell senescence and epithelial-mesenchymal transition.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Advanced drug delivery platforms targeting cellular senescence: A promising strategy for cancer therapy.Acta pharmaceutica Sinica. B · 2026Review
- Caloric restriction decelerates premature aging and cognitive decline in mice with deficient DNA repair.Communications biology · 2026Article
- Serum uric acid and its metabolism-a vital factor in the inflammatory transformation of cancer.Journal of advanced research · 2026Review
- Aging-Driven Immunosuppression: The Role of Tregs in the Ovarian Tumor Microenvironment.Aging cell · 2026Article
- Dispensable players: N-WASP and WASP are not crucial for homology-directed DNA repair.EMBO reports · 2026Article
- Exploring the Therapeutic Effect ofNutrients · 2026Article
- EYA4 promotes cellular senescence by enhancing P21 transcription through interaction with SIX2.Advanced biotechnology · 2026Article
- Serpine1 as a potential therapeutic target in pyrrolidine alkaloids-induced hepatic sinusoidal obstruction syndrome.JHEP reports : innovation in hepatology · 2026Article
- Colonic inflammatory response in a D-galactose-induced aging model: elevated IL-1β expression.Journal of molecular histology · 2026Article
- Engineered Clostridium butyricum-pMTL007-GLP-1 Delays Neurodegeneration in Prnp-SNCA*A53T Transgenic Mice Model by Suppressing Astrocyte Senescence.Probiotics and antimicrobial proteins · 2026Article
- A Review of Ionizing Radiation-Induced Senescence of Bone Marrow Mesenchymal Stem/Stromal Cells: Mechanisms and Therapeutic Strategies.Current issues in molecular biology · 2026Review
- The PARP inhibitor olaparib promotes senescence in murine macrophages.GeroScience · 2026Article
- Article
- The senescent niche hypothesis: microglial dysfunction and replacement strategies in drug-resistant epilepsy.Frontiers in immunology · 2026Review
155 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
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The genome is constantly attacked by genotoxic insults. DNA damage has long been established as a cause of cancer development through its mutagenic consequences. Conversely, radiation therapy and chemotherapy induce DNA damage to drive cells into apoptosis or senescence as outcomes of the DNA damage response (DDR). More recently, DNA damage has been recognized as a causal factor for the aging process. The role of DNA damage in aging and age-related diseases is illustrated by numerous congenital progeroid syndromes that are caused by mutations in genome maintenance pathways. During the past 2 decades, understanding how DDR drives cancer development and contributes to the aging process has progressed rapidly. It turns out that the DDR factor p53 takes center stage during tumor development and also plays an important role in the aging process. Studies in metazoan models ranging from
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.