ArticleMolecular cell2023
Genome homeostasis defects drive enlarged cells into senescence.
Article in Molecular cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 66 citations in OpenAlex.
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- Cell size-dependent mRNA transcription drives proteome remodeling.Cell reports · 2026Article
- Experimental evolution of cellular miniaturization reveals a putative mechanism for cell size evolution.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Cell size modulates ferroptosis susceptibility.eLife · 2026Article
- Induction of senescence like macrophages by hepatocellular carcinoma cells in vitro.Discover oncology · 2026Article
- Cell and Nuclear Size Is Associated with Chromosomal Instability and Tumorigenicity in Cancer Cells That Undergo Whole Genome Doubling.Cancer research · 2026Article
- Emerging Strategies to Inhibit the G1/S Transition for Cancer Therapy.Cancer research · 2026Review
- Endogenous Amplification of Apoptosis via p53 Regulation using a Cascade Nanocatalytic Medicine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cell size modulates ferroptosis susceptibility.bioRxiv : the preprint server for biology · 2026Article
- Cell enlargement drives aging-associated proteome remodeling and shortens replicative lifespan.bioRxiv : the preprint server for biology · 2026Article
- G1/S arrest: a key mechanism of cellular aging and replicative senescence.Biogerontology · 2026Review
- Cancer-associated USP28 missense mutations disrupt 53BP1 interaction and p53 stabilization.Nature communications · 2025Article
- Tumour Cell Size Control and Its Impact on Tumour Cell Function.Cell proliferation · 2025Review
- ESR1 Regulates Fecundity and Functions in Sheep Endometrial Stromal Cells.International journal of molecular sciences · 2025Article
- The G1/S transition in mammalian stem cells in vivo is autonomously regulated by cell size.Nature communications · 2025Article
- Conserved nucleocytoplasmic density homeostasis drives cellular organization across eukaryotes.Nature communications · 2025Article
- Enlarged PML-nuclear bodies trigger conflicting cell cycle signal-mediated cytotoxicity in leukemia cells.Cell death & disease · 2025Article
- The Molecular Interplay Between p53-Mediated Ferroptosis and Non-Coding RNAs in Cancer.International journal of molecular sciences · 2025Review
- Bibliometric insights into the cell cycle, aging, and metabolism: from molecular mechanisms to clinical implications.Biogerontology · 2025Review
- Nuclear morphometrics coupled with machine learning identifies dynamic states of senescence across age.Nature communications · 2025Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Cellular senescence refers to an irreversible state of cell-cycle arrest and plays important roles in aging and cancer biology. Because senescence is associated with increased cell size, we used reversible cell-cycle arrests combined with growth rate modulation to study how excessive growth affects proliferation. We find that enlarged cells upregulate p21, which limits cell-cycle progression. Cells that re-enter the cell cycle encounter replication stress that is well tolerated in physiologically sized cells but causes severe DNA damage in enlarged cells, ultimately resulting in mitotic failure and permanent cell-cycle withdrawal. We demonstrate that enlarged cells fail to recruit 53BP1 and other non-homologous end joining (NHEJ) machinery to DNA damage sites and fail to robustly initiate DNA damage-dependent p53 signaling, rendering them highly sensitive to genotoxic stress. We propose that an impaired DNA damage response primes enlarged cells for persistent replication-acquired damage, ultimately leading to cell division failure and permanent cell-cycle exit.
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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.