ArticleCell death & disease2018
Transcriptional repression of DNA repair genes is a hallmark and a cause of cellular senescence.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 66 citations in OpenAlex.
- Broad repression of DNA repair genes in senescent cells identified by integration of transcriptomic data.Nucleic acids research · 2025Pooled it
- Effects of High-Dose Ionizing Radiation in Human Gene Expression: A Meta-Analysis.International journal of molecular sciences · 2020Pooled it
- Loss of killifish cGAS attenuates age-related signatures but does not affect organismal life span.EMBO reports · 2026Article
- An integrated multi-algorithm analysis to decipher senescence and metabolic characteristics in nucleus pulposus cells during disc degeneration.GeroScience · 2026Article
- Fate Bifurcation of Cellular Senescence: Dynamic Regulation from Tumor Suppression to Recurrence Risk.Cells · 2026Review
- Necroptosis induced by MLKL overexpression in liver triggers cellular senescence and leads to chronic inflammation and fibrosis.GeroScience · 2026Article
- Cellular Senescence Triggered by Food and Environmental Genotoxins.International journal of molecular sciences · 2026Review
- Chromatin repression by PRC2 results in reduced gene expression driving key features of CD8 T cell exhaustion.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Therapy-induced senescence of glioblastoma cells is determined by the p21Cell death & disease · 2025Article
- Transcriptional activation of genes associated with the matrisome is a common feature of senescent endothelial cells.Biogerontology · 2025Article
- Comparative Transcriptome Analysis of Hens' Livers in Conventional Cage vs. Cage-Free Egg Production Systems.Veterinary medicine international · 2025Article
- Beyond polarization: macrophage senescence in immunoregulation and cancer therapy.International journal of biological sciences · 2025Review
- Senescence-like Phenotype After Chronic Exposure to Isoproterenol in Primary Quiescent Immune Cells.Biomolecules · 2024Article
- Decoding senescence of aging single cells at the nexus of biomaterials, microfluidics, and spatial omics.npj aging · 2024Review
- Uncoupling of mTORC1 from E2F activity maintains DNA damage and senescence.Nature communications · 2024Article
- Targeting DHX9 Triggers Tumor-Intrinsic Interferon Response and Replication Stress in Small Cell Lung Cancer.Cancer discovery · 2024Article
- Effects of p53 and ATRX inhibition on telomeric recombination in aging fibroblasts.Frontiers in oncology · 2024Article
- Article
- Article
- Modulation of Cellular Senescence in HEK293 and HepG2 Cells by Ultrafiltrates UPla and ULu Is Partly Mediated by Modulation of Mitochondrial Homeostasis under Oxidative Stress.International journal of molecular sciences · 2023Article
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence response is (i) activated by numerous stresses, (ii) is characterized by a stable proliferation arrest, and (iii) by a set of specific features. Timely regulated senescence is thought to be beneficial, whereas chronic senescence such as during normal or premature aging is deleterious as it favors most, if not all, age-related diseases. In this study, using in-house or publicly available microarray analyses of transcriptomes of senescent cells, as well as analyses of the level of expression of several DNA repair genes by RT-qPCR and immunoblot, we show that repression of DNA repair gene expression is associated with cellular senescence. This repression is mediated by the RB/E2F pathway and it may play a causal role in senescence induction, as single DNA repair gene repression by siRNA induced features of premature senescence. Importantly, activating RB independently of direct DNA damage also results in repression of DNA repair genes and in the subsequent induction of DNA damage and senescence. The dogma is that DNA damage observed during cellular senescence is directly provoked by DNA lesions following genotoxic attack (UV, IR, and ROS) or by induction of replicative stress upon oncogenic activation. Our in vitro results support a largely unsuspected contribution of the loss of DNA repair gene expression in the induction and the accumulation of the DNA damage observed in most, if not all, kinds of cellular senescence, and thus in the induction of cellular senescence. Further demonstration using in vivo models will help to generalize our findings.
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.