ReviewNature reviews. Rheumatology2023
Inflammation and DNA damage: cause, effect or both.
Review in Nature reviews. Rheumatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 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
119 citing papers in PubMed, 170 citations in OpenAlex.
- Punicalagin alleviates senile osteoporosis by inhibiting the senescence of bone mesenchymal stem cells via NRF2/HO-1 pathway.Regenerative therapy · 2026Article
- ANGPTL8 induces the aging of hematopoietic stem/progenitor cells.Biogerontology · 2026Article
- DNA Damage in Placental and Fetal Cells in Rats with Perinatal Immune Activation.Bulletin of experimental biology and medicine · 2026Article
- Sperm DNA fragmentation and its influence on mammalian reproduction.Nature reviews. Urology · 2026Review
- Aging in Spaceflight, Oxidative Stress, and Microbiome Dysbiosis: A Comprehensive Review.International journal of molecular sciences · 2026Review
- miRNA-mediated cell-to-cell communications boost DNA repair during the radioadaptive response.Nucleic acids research · 2026Article
- Cellular senescence and aging: molecular mechanisms and convergent pathways.Cellular and molecular life sciences : CMLS · 2026Review
- Beyond apoptosis: nanomedicine enabled reprogramming of tumor cell death for next-generation radiosensitization.Journal of nanobiotechnology · 2026Review
- Endometritis and endometrial fibrosis are associated with alterations in mare endometrial proteome.BMC veterinary research · 2026Article
- Effect of Probiotic Supplementation in Older Individuals with Mild Cognitive Impairment and Alzheimer's Disease: A Randomized, Placebo-Controlled, Triple-Blind Clinical Trial.Probiotics and antimicrobial proteins · 2026Article
- From inflammation to malignancy: the dynamic evolution of cancer-associated fibroblasts in IBD-CRC.Neoplasia (New York, N.Y.) · 2026Review
- A programmable platform enabling targeted chromosome substitution and cross-species stability profiling.Protein & cell · 2026Article
- Deciphering the Shared Mechanisms Underlying the Effects of Osthole on the Inflammation-Cancer Axis: An Integrative Network Pharmacology and Molecular Dynamics Study.Current issues in molecular biology · 2026Article
- Facilitated DNA damage repair as an emerging therapeutic strategy for inflammatory and fibrotic diseases.RSC chemical biology · 2026Review
- Hierarchies of resistance to DNA damage response inhibitors: from pathway restoration to replication stress tolerance.Experimental hematology & oncology · 2026Review
- TOP2 and NOS2 Orchestrate the Generation of DNA Breaks to Promote Colitis Cancer Initiation.Cancers · 2026Article
- Role of hypertrophic adipocytes, collagen VI, and CD38 in adipose tissue fibrosis in obesity.Scientific reports · 2026Article
- Multi-tissue analysis identifies mitochondrial genes in chicken aging-induced productivity decline.Journal of animal science and biotechnology · 2026Article
- IL-1-mediated inflammation promotes metastatic dissemination and resistance to EGFR-targeted therapy.NPJ precision oncology · 2026Article
- Epithelial MST1 deficiency promotes pyroptosis and aggravates inflammatory bowel disease via the YAP/p73 signaling pathway.Cell death and differentiation · 2026Article
59 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 at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation is a biological response involving immune cells, blood vessels and mediators induced by endogenous and exogenous stimuli, such as pathogens, damaged cells or chemicals. Unresolved (chronic) inflammation is characterized by the secretion of cytokines that maintain inflammation and redox stress. Mitochondrial or nuclear redox imbalance induces DNA damage, which triggers the DNA damage response (DDR) that is orchestrated by ATM and ATR kinases, which modify gene expression and metabolism and, eventually, establish the senescent phenotype. DDR-mediated senescence is induced by the signalling proteins p53, p16 and p21, which arrest the cell cycle in G1 or G2 and promote cytokine secretion, producing the senescence-associated secretory phenotype. Senescence and inflammation phenotypes are intimately associated, but highly heterogeneous because they vary according to the cell type that is involved. The vicious cycle of inflammation, DNA damage and DDR-mediated senescence, along with the constitutive activation of the immune system, is the core of an evolutionarily conserved circuitry, which arrests the cell cycle to reduce the accumulation of mutations generated by DNA replication during redox stress caused by infection or inflammation. Evidence suggests that specific organ dysfunctions in apparently unrelated diseases of autoimmune, rheumatic, degenerative and vascular origins are caused by inflammation resulting from DNA damage-induced senescence.
Indexed as
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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.