ArticleAging cell2025
Large-Scale Clustered Transcriptional Silencing Associated With Cellular Senescence.
Article in Aging cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed.
- UHRF1 overexpression generates distinct senescent states with different Tp53 dependencies.EMBO reports · 2026Article
- From aging biology to cardiac biotechnology: emerging platforms for modeling cardiac aging.JCI insight · 2026Review
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- Baicalin affects the progression of diabetic retinopathy through the RAGE/PXDN/PI3K/AKT pathway.Journal of translational medicine · 2025Article
- Space radiation induces distinct senescent phenotypes: Implications for space travel.npj aging · 2025Article
- SIRT1 Prevents Lens Epithelial Cell Senescence During Age-Related Cataract via Regulating p66Shc.Aging cell · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Senescence is a cell fate associated with age-related pathologies; however, senescence markers are not well-defined. Using single cell multi-isotope imaging mass spectrometry (MIMS), we identified hypercondensed, transcriptionally silent DNA globules in a senescence model induced by dysfunctional telomeres. This architectural phenomenon was associated with geographically clustered transcriptional repression across somatic chromosomes with over-representation of cell cycle genes. Senescence-stimuli was associated with a higher frequency of cells that exhibited geographically concentrated transcriptional repression relative to control cells. This phenomenon was also observed in multiple other senescence models, including replicative senescence and irradiation. We further identified an enrichment of common pathways in all models of senescence, suggesting a common cellular response to this silencing phenomenon. Such large-scale clustered silencing of chromosomal segments rather than individual genes may explain senescence heterogeneity and a putative trajectory toward deep, irreversible 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.