ArticleNature communications2018
FoxM1 repression during human aging leads to mitotic decline and aneuploidy-driven full senescence.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.
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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.
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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
85 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.
- Broad repression of DNA repair genes in senescent cells identified by integration of transcriptomic data.Nucleic acids research · 2025Pooled it
- Ionizing radiation induces senescence of dermal papilla cells through inhibiting the FOXM1-KIF20A pathway.Genes & diseases · 2027Article
- Article
- A tumour-host feed-forward loop contributes to the growth of chromosomal instability-induced tumours.EMBO reports · 2026Article
- A microprotein encoded by FERMT3 modulates endothelial cell protein catabolism and induces cell cycle arrest and senescence.Cell communication and signaling : CCS · 2026Article
- Article
- IVNS1ABP mutation drives cellular senescence in newly identified progeroid neuropathy.Nature communications · 2026Article
- Article
- 5-HEPE Ameliorates Aging of Duck Ovarian Granulosa Cells by Targeting FOXM1 and Suppressing Oxidative Stress.Antioxidants (Basel, Switzerland) · 2025Article
- Human fibroblasts from aged individuals exhibit chromosomal instability through replication stress caused by oxidative stress.npj aging · 2025Article
- Cancer and Aging Biomarkers: Classification, Early Detection Technologies and Emerging Research Trends.Biosensors · 2025Review
- The Mechanism and Potential Therapeutic Strategies of Vascular Aging.Aging medicine (Milton (N.S.W)) · 2025Review
- Gene therapy strategies for aging intervention.Cell insight · 2025Review
- Exploring the Single-Cell Dynamics of FOXM1 Under Cell Cycle Perturbations.Cell proliferation · 2025Article
- DNA methylation protects cancer cells against senescence.Nature communications · 2025Article
- FOXM1 expression reverts aging chromatin profiles through repression of the senescence-associated pioneer factor AP-1.Nature communications · 2025Article
- Replicative senescence in amniotic fluid-derived mesenchymal stem cells and its impact on their immunomodulatory properties.Histochemistry and cell biology · 2025Article
- Proteogenomic analysis reveals adaptive strategies for alleviating the consequences of aneuploidy in cancer.The EMBO journal · 2025Article
- Centromere inactivation during aging can be rescued in human cells.Molecular cell · 2025Article
- Chromosome mis-segregation triggers cell cycle arrest through a mechanosensitive nuclear envelope checkpoint.Nature cell biology · 2025Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aneuploidy, an abnormal chromosome number, has been linked to aging and age-associated diseases, but the underlying molecular mechanisms remain unknown. Here we show, through direct live-cell imaging of young, middle-aged, and old-aged primary human dermal fibroblasts, that aneuploidy increases with aging due to general dysfunction of the mitotic machinery. Increased chromosome mis-segregation in elderly mitotic cells correlates with an early senescence-associated secretory phenotype (SASP) and repression of Forkhead box M1 (FoxM1), the transcription factor that drives G2/M gene expression. FoxM1 induction in elderly and Hutchison-Gilford progeria syndrome fibroblasts prevents aneuploidy and, importantly, ameliorates cellular aging phenotypes. Moreover, we show that senescent fibroblasts isolated from elderly donors' cultures are often aneuploid, and that aneuploidy is a key trigger into full senescence phenotypes. Based on this feedback loop between cellular aging and aneuploidy, we propose modulation of mitotic efficiency through FoxM1 as a potential strategy against aging and progeria syndromes.
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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.