ArticleAging2014
A role for SUV39H1-mediated H3K9 trimethylation in the control of genome stability and senescence in WI38 human diploid lung fibroblasts.
Article in Aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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
25 citing papers in PubMed, 48 citations in OpenAlex.
- Review
- Mechanical Stress Triggers Premature Senescence in Cardiac Fibroblasts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Reactivation of retrotransposable elements is associated with environmental stress and ageing.Nature reviews. Genetics · 2025Review
- The Information Theory of Aging.Nature aging · 2023Review
- Epigenetic regulation of mesenchymal stem cell aging through histone modifications.Genes & diseases · 2023Review
- Parallel shift of DNA methylation and gene expression toward the mean in mouse spleen with aging.Aging · 2023Article
- Impact of Environmental and Epigenetic Changes on Mesenchymal Stem Cells during Aging.International journal of molecular sciences · 2023Review
- Single-cell epigenome analysis reveals age-associated decay of heterochromatin domains in excitatory neurons in the mouse brain.Cell research · 2022Article
- Epigenetics, DNA damage, and aging.The Journal of clinical investigation · 2022Review
- CD8+T cell responsiveness to anti-PD-1 is epigenetically regulated by Suv39h1 in melanomas.Nature communications · 2022Article
- Review
- CBX4 Regulates Replicative Senescence of WI-38 Fibroblasts.Oxidative medicine and cellular longevity · 2022Article
- Stress-Induced Epigenetic Changes in Hippocampal Mkp-1 Promote Persistent Depressive Behaviors.Molecular neurobiology · 2019Article
- PLZF limits enhancer activity during hematopoietic progenitor aging.Nucleic acids research · 2019Article
- RFX1 downregulation contributes to TLR4 overexpression in CD14Clinical epigenetics · 2019Article
- A regulatory circuitry comprising TP53,Bioscience reports · 2018Article
- Adverse effects of paternal chemotherapy exposure on the progeny brain: intergenerational chemobrain.Oncotarget · 2018Article
- Baicalin hydrate inhibits cancer progression in nasopharyngeal carcinoma by affecting genome instability and splicing.Oncotarget · 2018Article
- Abnormal Epigenetic Regulation of Immune System during Aging.Frontiers in immunology · 2018Review
- Epigenetic Regulation of Cellular Senescence and Aging.Frontiers in genetics · 2017Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence has been associated with the age-dependent decline in tissue repair and regeneration, the increasing deterioration of the immune system, and the age-dependent increase in the incidence of cancer. Here, we show that senescence of human lung fibroblast WI-38 cells is associated with extensive changes to the gene expression profile, including the differential expression of transcriptional and epigenetic regulators. Among those,SUV39H1 was downregulated in senescent cells, correlated with a decrease in global H3K9 trimethylation, reduced H3K9me3 levels in repetitive DNA sequence regions such as satellites and transposable elements, and increased transcription of these repetitive DNA sequences. This indicates that SUV39H1 plays a role in limiting genomic instability in dividing cells and suggests that SUV39H1 downregulation may contribute to the establishment of senescence by increasing genomic instability. Additionally, the manipulation of SUV39H1 expression levels resulted in altered cell cycle distribution, suggesting a causal role of SUV39H1 in the establishment of cellular senescence. Thus, based on our findings and the results from previous reports, we propose a model in which SUV39H1 downregulation promotes the establishment of cellular senescence.
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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.