ArticleNature aging2022
Locus-specific induction of gene expression from heterochromatin loci during cellular senescence.
Article in Nature aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 27 citations in OpenAlex.
- Systemic epigenetic dysregulation as a driver of ageing and a therapeutic target.Nature reviews. Molecular cell biology · 2026Review
- Review
- The rise of RAS: how gradual oncogene activation shapes the OIS spectrum.Genes & development · 2025Review
- A guide to studying 3D genome structure and dynamics in the kidney.Nature reviews. Nephrology · 2025Review
- Dynamic 3D genome reorganization during senescence: defining cell states through chromatin.Cell death and differentiation · 2025Article
- Variation in the Content of Three Tandem Repeats of the Human Genome (Ribosomal, Satellite III, and Telomere) in Peripheral Blood Leukocyte DNA of People of Different Ages (5-101 Years).Journal of aging research · 2025Article
- A cellular identity crisis? Plasticity changes during aging and rejuvenation.Genes & development · 2024Review
- Article
- HMGA1 orchestrates chromatin compartmentalization and sequesters genes into 3D networks coordinating senescence heterogeneity.Nature communications · 2024Article
- Regulation of cell function and identity by cellular senescence.The Journal of cell biology · 2024Review
- Determining the Compaction State of Genes Using DNA FISH.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Imaging-based chromatin and epigenetic age, ImAge, quantitates aging and rejuvenation.Research square · 2023Article
- KDM4C-mediated senescence defense is a targetable vulnerability in gastric cancer harboring TP53 mutations.Clinical epigenetics · 2023Article
- Chromatin conformational changes at human satellite II contribute to the senescence phenotype in the tumor microenvironment.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Chromatin: the old and young of it.Frontiers in molecular biosciences · 2023Review
- BMAL1 moonlighting as a gatekeeper for LINE1 repression and cellular senescence in primates.Nucleic acids research · 2022Article
- Mitochondria and sensory processing in inflammatory and neuropathic pain.Frontiers in pain research (Lausanne, Switzerland) · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
20 authors at 8 institutions in 4 countries.
Funding
Abstract
Senescence is a fate-determined state, accompanied by reorganization of heterochromatin. Although lineage-appropriate genes can be temporarily repressed through facultative heterochromatin, stable silencing of lineage-inappropriate genes often involves the constitutive heterochromatic mark, histone H3 lysine 9 trimethylation (H3K9me3). The fate of these heterochromatic genes during senescence is unclear. In the present study, we show that a small number of lineage-inappropriate genes, exemplified by the LCE2 skin genes, are derepressed during senescence from H3K9me3 regions in fibroblasts. DNA FISH experiments reveal that these gene loci, which are condensed at the nuclear periphery in proliferative cells, are decompacted during senescence. Decompaction of the locus is not sufficient for LCE2 expression, which requires p53 and C/EBPβ signaling. NLRP3, which is predominantly expressed in macrophages from an open topologically associated domain (TAD), is also derepressed in senescent fibroblasts due to the local disruption of the H3K9me3-rich TAD that contains it. NLRP3 has been implicated in the amplification of inflammatory cytokine signaling in senescence and aging, highlighting the functional relevance of gene induction from 'permissive' H3K9me3 regions in senescent cells.
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.