Evidence map›Paper›PMID 40562791›Full record

ArticleEMBO reports2025

JMJD3-mediated senescence is required to overcome stress-induced hematopoietic defects.

Yuichiro Nakata, Takeshi Ueda, Yasuyuki Sera, Miho Koizumi, Katsutoshi Imamura, Akinori Kanai, Ken-Ichiro Ikeda, Norimasa Yamasaki, Akiko Nagamachi, Kohei Kobatake and 10 more

Erratum issuedAbstract read
In one paragraph

Article in EMBO reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. A cross-talk between p16High senescence and cellular reprogramming.Clinical science (London, England : 1979) · 2026
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors.

Yuichiro NakataDepartment of Systems Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan. nakatay@chiba-u.jp.ORCID 0000-0002-6852-4201
Takeshi UedaDepartment of Biochemistry, Faculty of Medicine, Kindai University, Osakasayama, Japan.ORCID 0000-0001-9823-6764
Yasuyuki SeraField of Human Disease Models, Major in Advanced Life Sciences and Medicine, Institute of Laboratory Animals, Tokyo Women's Medical University, Tokyo, Japan.
Miho KoizumiField of Human Disease Models, Major in Advanced Life Sciences and Medicine, Institute of Laboratory Animals, Tokyo Women's Medical University, Tokyo, Japan.
Katsutoshi ImamuraDepartment of Systems Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Akinori KanaiLaboratory of Systems Genomics, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Chiba, Japan.ORCID 0000-0003-1555-6768
Ken-Ichiro IkedaDepartment of Urology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.ORCID 0000-0002-3174-8738
Norimasa YamasakiDepartment of Disease Model, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Akiko NagamachiDepartment of Animal Experimentation, Foundation for Biomedical Research and Innovation at Kobe, Kobe city, Japan.
Kohei KobatakeDepartment of Urology, Institute of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Masataka TaguchiDepartment of Hematology, Atomic Bomb Disease Institute, Nagasaki University, Nagasaki, Japan.ORCID 0000-0002-0642-5814
Yusuke SotomaruNatural Science Center for Basic Research and Development, Hiroshima University, Hiroshima, Japan.ORCID 0000-0002-2856-1518
Tatsuo IchinoheDepartment of Hematology and Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Zen-Ichiro HondaDepartment of Beauty & Wellness, Professional University of Beauty & Wellness, Yokohama, Japan.
Takuro NakamuraDepartment of Experimental Pathology, Institute of Medical Science, Tokyo Medical University, Tokyo, Japan.
Ichiro ManabeDepartment of Systems Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
Toshio SudaInstitute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Bei Jing Shi, China.
Keiyo TakuboDepartment of Cell Fate Biology and Stem Cell Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.ORCID 0000-0002-1736-7592
Osamu KaminumaDepartment of Disease Model, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Hiroaki HondaField of Human Disease Models, Major in Advanced Life Sciences and Medicine, Institute of Laboratory Animals, Tokyo Women's Medical University, Tokyo, Japan. honda.hiroaki@twmu.ac.jp.ORCID 0000-0002-4617-9670

Funding

AMED-CREST 25gm131006
6 · The paper itself

Abstract

Cellular senescence in stem cells compromises regenerative capacity, promotes chronic inflammation, and is implicated in aging. Hematopoietic stem and progenitor cells (HSPCs) are responsible for producing mature blood cells, however, how cellular senescence influences their function is largely unknown. Here, we show that JMJD3, a histone demethylase, activates cellular senescence by upregulating p16

Indexed as

Cellular SenescenceHematopoiesisHematopoietic Stem CellsJumonji Domain-Containing Histone DemethylasesStress, PhysiologicalAnimalsCyclin-Dependent Kinase Inhibitor p16Epigenesis, GeneticHistonesHumansMiceMice, KnockoutWnt Signaling PathwayCyclin-Dependent Kinase Inhibitor p16HistonesJumonji Domain-Containing Histone DemethylasesKdm6b protein, mouseCellular senescenceHematopoietic stem cellHistone demethylaseStress hematopoiesis

Identifiers

PMID40562791
PMCPMC12331899

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.