Evidence map›Paper›PMID 42276063›Full record

ArticleStem cell reports2026

Suppression of ATM kinase signaling accelerates cellular senescence.

Kei-Ichi Ishikawa, Takahiro Shiga, Takumi Hirose, Naoko Kuzumaki, Sakura Miyoshi, Akihiro Yamaguchi, Hidetaka Tamune, Avijite Kumer Sarkar, Kento Nakai, Kazuyoshi Baba and 4 more

Abstract read
In one paragraph

Article in Stem cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Kei-Ichi IshikawaCenter for Genomic and Regenerative Medicine, Juntendo University School of Medicine, Tokyo, Japan; Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan. Electronic address: kishikaw@juntendo.ac.jp.
Takahiro ShigaCenter for Genomic and Regenerative Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Takumi HiroseCenter for Genomic and Regenerative Medicine, Juntendo University School of Medicine, Tokyo, Japan.
Naoko KuzumakiDepartment of Physiology, Keio University School of Medicine, Tokyo, Japan.
Sakura MiyoshiDepartment of Physiology, Keio University School of Medicine, Tokyo, Japan.
Akihiro YamaguchiCenter for Genomic and Regenerative Medicine, Juntendo University School of Medicine, Tokyo, Japan; Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Hidetaka TamuneDepartment of Cellular Neurobiology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Avijite Kumer SarkarDepartment of Prosthodontics, School of Dentistry, Showa University, Tokyo, Japan.
Kento NakaiDepartment of Prosthodontics, School of Dentistry, Showa University, Tokyo, Japan.
Kazuyoshi BabaDepartment of Prosthodontics, School of Dentistry, Showa University, Tokyo, Japan.
Shigeo OkabeDepartment of Cellular Neurobiology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Nobutaka HattoriCenter for Genomic and Regenerative Medicine, Juntendo University School of Medicine, Tokyo, Japan; Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan; Neurodegenerative Disorders Collaborative Laboratory, RIKEN Center for Brain Science, Wako, Saitama, Japan.
Hideyuki OkanoDepartment of Physiology, Keio University School of Medicine, Tokyo, Japan.
Wado AkamatsuCenter for Genomic and Regenerative Medicine, Juntendo University School of Medicine, Tokyo, Japan. Electronic address: awado@juntendo.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cells derived from rejuvenated human induced pluripotent stem cells (hiPSCs) require extended culture periods to achieve functional maturation, and it remains difficult to recapitulate cellular senescence in these cells in vitro. This limitation hinders the accurate and efficient modeling of age-related neurodegenerative diseases. Here, we aimed to establish a simple approach to promote neuronal maturation and improve the efficiency of hiPSC-based disease modeling. Using a small-molecule inhibitor library, we identified an ATM kinase inhibitor, KU60019, that promotes both maturation-associated features and senescence-associated phenotypes in hiPSC-derived neurons and fibroblasts. KU60019 treatment promoted the manifestation of disease-relevant phenotypes in hiPSC models of age-related neurodegenerative diseases. Furthermore, senolytic analyses suggested that KU60019-induced senescent cells depend on pro-survival pathways, including HSP90-associated signaling. These findings suggest that KU60019 provides a simple and useful tool for accelerating phenotypic recapitulation in hiPSC models of age-related neurodegenerative diseases.

Indexed as

Ataxia Telangiectasia Mutated ProteinsCellular SenescenceSignal TransductionCell DifferentiationFibroblastsHumansInduced Pluripotent Stem CellsNeuronsProtein Kinase InhibitorsAtaxia Telangiectasia Mutated ProteinsATM protein, humanProtein Kinase InhibitorsAlzheimer’s diseaseATM kinasecellular senescencehuman induced pluripotent stem cellsKU60019neurodegenerative disease modelingneuronal maturationParkinson’s disease

Identifiers

PMID42276063
PMCPMC13385434

What OpenQuestion holds

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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.