ArticleNucleic acids research2020
Senescence-activated enhancer landscape orchestrates the senescence-associated secretory phenotype in murine fibroblasts.
Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 71 citations in OpenAlex.
- Genomic, epigenomic and transcriptomic regulation of cellular senescence.Nature reviews. Genetics · 2026Review
- Aging-associated SATB1 deficiency remodels 3D genome architecture and transcriptional programs in naive CD4Science advances · 2026Article
- From cell to disease: Regulatory networks and mechanisms of super‑enhancers in aging (Review).Molecular medicine reports · 2026Review
- Neutrophil-to-high-density lipoprotein cholesterol ratio and prevalent cardiometabolic multimorbidity in older adults: an exploratory cross-sectional analysis.BMC endocrine disorders · 2026Article
- SenFlag gene signature identifies senescent cells in mouse and human tissues through a conserved core transcriptional program.The EMBO journal · 2026Article
- Systemic epigenetic dysregulation as a driver of ageing and a therapeutic target.Nature reviews. Molecular cell biology · 2026Review
- Age-independent and targetable transcription factor networks regulating CD8Cell reports · 2026Article
- Spatial Reorganization of Chromatin Architecture Shapes the Expression Phenotype of Therapy-Induced Senescent Cells.Aging cell · 2026Article
- Blocking nuclear receptor Nr4a3 unlocks the senescence barrier to promote direct cardiac reprogramming.Science advances · 2025Article
- TP63 mediates the generation of tumour-specific chromatin loops that underlie MYC activation in radiation-induced tumorigenesis.Nature communications · 2025Article
- Aging-Related Mechanisms Underlying Carcinogenesis: Therapeutic Opportunities.Aging and disease · 2025Review
- Review
- Ligand-specific regulation of a binary enhancer code dictating cellular senescence.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Inhibiting the Histone Demethylase Kdm4a Restrains Cardiac Fibrosis After Myocardial Infarction by Promoting Autophagy in Premature Senescent Fibroblasts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- FOXM1 expression reverts aging chromatin profiles through repression of the senescence-associated pioneer factor AP-1.Nature communications · 2025Article
- Immunosenescence promotes cancer development: from mechanisms to treatment strategies.Cell communication and signaling : CCS · 2025Review
- Exploring the link between fat-soluble vitamins and aging-associated immune system status: a literature review.Immunity & ageing : I & A · 2025Review
- A guide to studying 3D genome structure and dynamics in the kidney.Nature reviews. Nephrology · 2025Review
- Associations between Life's Essential 8 scores and systemic immune-inflammation index among American-adult populations without cardiovascular disease.Frontiers in medicine · 2025Article
- Genetic overlap between breast cancer and sarcopenia: exploring the prognostic implications of SLC38A1 gene expression.BMC cancer · 2024Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The three-dimensional configuration of the chromatin architecture is known to be crucial for alterations in the transcriptional network; however, the underlying mechanisms of epigenetic control of senescence-related gene expression by modulating the chromatin architecture remain unknown. Here, we demonstrate frequent chromosomal compartment switching during mouse embryonic fibroblasts (MEFs) replicative senescence as characterized by senescence-inactivated (SIAEs) and -activated enhancers (SAEs) in topologically associated domains (TADs). Mechanistically, SAEs are closely correlated with senescence-associated secretory phenotype (SASP) genes, which are a key transcriptional feature of an aging microenvironment that contributes to tumor progression, aging acceleration, and immunoinflammatory responses. Moreover, SAEs can positively regulate robust changes in SASP expression. The transcription factor CCAAT/enhancer binding protein α (C/EBPα) is capable of enhancing SAE activity, which accelerates the emergence of SAEs flanking SASPs and the secretion of downstream factors, contributing to the progression of senescence. Our results provide novel insight into the TAD-related control of SASP gene expression by revealing hierarchical roles of the chromatin architecture, transcription factors, and enhancer activity in the regulation 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.