ArticleNature communications2022
Senescent cells limit p53 activity via multiple mechanisms to remain viable.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 37 citations in OpenAlex.
- Cellular senescence and regulated cell death in cancer: mechanisms, cross-regulatory networks and therapeutic implications.Journal of hematology & oncology · 2026Review
- From cell to disease: Regulatory networks and mechanisms of super‑enhancers in aging (Review).Molecular medicine reports · 2026Review
- Cellular senescence links muscle atrophy and posttraumatic osteoarthritis after ACL injury.Function (Oxford, England) · 2026Article
- Senolytic Changes in Murine Arteriovenous Fistulas with CKD.Kidney360 · 2026Article
- CHK2-USP37 axis stabilizes FOXO4 to sustain senescence and evade apoptosis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- DNA damage drives a unique, Alzheimer's disease-relevant senescent state in neurons.bioRxiv : the preprint server for biology · 2026Article
- Cell Type-Specific Expression of p16, p21, and p53 Reveals Age-Dependent Glial Senescence in the AppAging cell · 2026Article
- Ribonuclease 4 Functions in Nociceptor-Mediated Nerve Homeostasis.Nature communications · 2026Article
- Histone modification clocks for robust cross-species biological age prediction and elucidating senescence regulation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Cellular senescence and senolytic therapy in traumatic brain injury.Frontiers in neuroscience · 2026Review
- Inhibition of MCL-1 to eliminate senescent cells and mitigate renal fibrosis in aristolochic acid nephropathy.Cell death & disease · 2025Article
- Reduction of lymphotoxin beta receptor induces cellular senescence via the MDMX-p53 pathway.Cell death discovery · 2025Article
- A transcriptome-based human universal senescence index (hUSI) robustly predicts cellular senescence under various conditions.Nature aging · 2025Article
- p53 enhances DNA repair and suppresses cytoplasmic chromatin fragments and inflammation in senescent cells.Nature communications · 2025Article
- The impact of cellular senescence on aging skeletal muscle.Frontiers in cell and developmental biology · 2025Review
- Spinster homolog 2 (SPNS2) deficiency drives endothelial cell senescence and vascular aging via promoting pyruvate metabolism mediated mitochondrial dysfunction.Cell communication and signaling : CCS · 2024Article
- Review
- The chromatin accessibility and transcriptomic landscape of the aging mice cochlea and the identification of potential functional super-enhancers in age-related hearing loss.Clinical epigenetics · 2024Article
- Review
- Unraveling the complexity of the senescence-associated secretory phenotype in adamantinomatous craniopharyngioma using multimodal machine learning analysis.Neuro-oncology · 2024Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Super-enhancers regulate genes with important functions in processes that are cell type-specific or define cell identity. Mouse embryonic fibroblasts establish 40 senescence-associated super-enhancers regardless of how they become senescent, with 50 activated genes located in the vicinity of these enhancers. Here we show, through gene knockdown and analysis of three core biological properties of senescent cells that a relatively large number of senescence-associated super-enhancer-regulated genes promote survival of senescent mouse embryonic fibroblasts. Of these, Mdm2, Rnase4, and Ang act by suppressing p53-mediated apoptosis through various mechanisms that are also engaged in response to DNA damage. MDM2 and RNASE4 transcription is also elevated in human senescent fibroblasts to restrain p53 and promote survival. These insights identify key survival mechanisms of senescent cells and provide molecular entry points for the development of targeted therapeutics that eliminate senescent cells at sites of pathology.
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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.