Evidence map›Paper›PMID 39397009›Full record

ArticleCell death discovery2024

Polyploidy mitigates the impact of DNA damage while simultaneously bearing its burden.

Kazuki Hayashi, Kisara Horisaka, Yoshiyuki Harada, Yuta Ogawa, Takako Yamashita, Taku Kitano, Masahiro Wakita, Takahito Fukusumi, Hidenori Inohara, Eiji Hara and 1 more

Abstract read
In one paragraph

Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed.

  1. A transcription factor regulates development of a bacteria-housing eukaryotic cell through DNA damage mitigation.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Review
  3. Article
  4. Somatic mutations and genome mosaicism in aging and disease.Experimental & molecular medicine · 2026
    Review
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  6. Article
  7. Review
  8. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Kazuki HayashiDepartment of Molecular Biology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.ORCID http://orcid.org/0000-0003-4126-7505
Kisara HorisakaDepartment of Molecular Biology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Yoshiyuki HaradaDepartment of Molecular Biology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Yuta OgawaDepartment of Molecular Biology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Takako YamashitaDepartment of Molecular Biology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Taku KitanoDepartment of Molecular Biology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Masahiro WakitaDepartment of Molecular Biology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Takahito FukusumiDepartment of Otorhinolaryngology-Head and Neck Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Hidenori InoharaDepartment of Otorhinolaryngology-Head and Neck Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Eiji HaraDepartment of Molecular Biology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan. ehara@biken.osaka-u.ac.jp.ORCID http://orcid.org/0000-0001-7821-3960
Tomonori MatsumotoDepartment of Molecular Biology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan. matsumoto.tomonori.fbs@osaka-u.ac.jp.ORCID http://orcid.org/0000-0003-4483-2178

Funding

Japan Agency for Medical Research and Development (AMED) JP22fk0210099MEXT | Japan Science and Technology Agency (JST) JPMJFR2212MEXT | Japan Society for the Promotion of Science (JSPS) JP21K15974
6 · The paper itself

Abstract

Polyploidy is frequently enhanced under pathological conditions, such as tissue injury and cancer in humans. Polyploidization is critically involved in cancer evolution, including cancer initiation and the acquisition of drug resistance. However, the effect of polyploidy on cell fate remains unclear. In this study, we explored the effects of polyploidization on cellular responses to DNA damage and cell cycle progression. Through various comparisons based on ploidy stratifications of cultured cells, we found that polyploidization and the accumulation of genomic DNA damage mutually induce each other, resulting in polyploid cells consistently containing more genomic DNA damage than diploid cells under both physiological and stress conditions. Notably, despite substantial DNA damage, polyploid cells demonstrated a higher tolerance to its impact, exhibiting delayed cell cycle arrest and reduced secretion of inflammatory cytokines associated with DNA damage-induced senescence. Consistently, in mice with ploidy tracing, hepatocytes with high ploidy appeared to potentially persist in the damaged liver, while being susceptible to DNA damage. Polyploidy acts as a reservoir of genomic damage by mitigating the impact of DNA damage, while simultaneously enhancing its accumulation.

Identifiers

PMID39397009
PMCPMC11471775

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LicenceCC BY
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Registered trials

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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.