ArticlePloS one2019
Elimination of protein aggregates prevents premature senescence in human trisomy 21 fibroblasts.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Identification of the Down Syndrome Critical Region 3 Gene as a Mammalian Cell Size Regulator.Genes to cells : devoted to molecular & cellular mechanisms · 2026Article
- Interplay between DYRK1A dosage and aneuploidy-induced neuropathology in Down syndrome.Communications biology · 2026Article
- Chromosome duplication causes premature aging via defects in ribosome quality control.PLoS biology · 2025Article
- Elevated Senescence Markers in Developing Trisomy 21 Human Lungs.American journal of respiratory cell and molecular biology · 2025Article
- Premature aging in aneuploid yeast is caused in part by aneuploidy-induced defects in Ribosome Quality Control.bioRxiv : the preprint server for biology · 2024Article
- ABCA7 deficiency causes neuronal dysregulation by altering mitochondrial lipid metabolism.Molecular psychiatry · 2024Article
- Consequences of chromosome gain: A new view on trisomy syndromes.American journal of human genetics · 2022Review
- Cellular senescence and senolytics: the path to the clinic.Nature medicine · 2022Review
- Large-scale organoid study suggests effects of trisomy 21 on early fetal neurodevelopment are more subtle than variability between isogenic lines and experiments.Frontiers in neuroscience · 2022Article
- Restoration of keratinocytic phenotypes in autonomous trisomy-rescued cells.Stem cell research & therapy · 2021Article
- Building the Future Therapies for Down Syndrome: The Third International Conference of the T21 Research Society.Molecular syndromology · 2021Article
- A human isogenic iPSC-derived cell line panel identifies major regulators of aberrant astrocyte proliferation in Down syndrome.Communications biology · 2021Article
- The Study of Alternative Splicing Events in Human Induced Pluripotent Stem Cells From a Down's Syndrome Patient.Frontiers in cell and developmental biology · 2021Article
- Role of gut microbiota in epigenetic regulation of colorectal Cancer.Biochimica et biophysica acta. Reviews on cancer · 2021Review
- 4-Phenylbutyrate ameliorates apoptotic neural cell death in Down syndrome by reducing protein aggregates.Scientific reports · 2020Article
- Down syndrome: A curative prospect?AIMS neuroscience · 2020Review
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromosome abnormalities induces profound alterations in gene expression, leading to various disease phenotypes. Recent studies on yeast and mammalian cells have demonstrated that aneuploidy exerts detrimental effects on organismal growth and development, regardless of the karyotype, suggesting that aneuploidy-associated stress plays an important role in disease pathogenesis. However, whether and how this effect alters cellular homeostasis and long-term features of human disease are not fully understood. Here, we aimed to investigate cellular stress responses in human trisomy syndromes, using fibroblasts and induced pluripotent stem cells (iPSCs). Dermal fibroblasts derived from patients with trisomy 21, 18 and 13 showed a severe impairment of cell proliferation and enhanced premature senescence. These phenomena were accompanied by perturbation of protein homeostasis, leading to the accumulation of protein aggregates. We found that treatment with sodium 4-phenylbutyrate (4-PBA), a chemical chaperone, decreased the protein aggregates in trisomy fibroblasts. Notably, 4-PBA treatment successfully prevented the progression of premature senescence in secondary fibroblasts derived from trisomy 21 iPSCs. Our study reveals aneuploidy-associated stress as a potential therapeutic target for human trisomies, including Down syndrome.
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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.