Evidence map›Paper›PMID 40972586›Full record

ArticleStem cell reports2025

Signaling pathway-based culture condition improves differentiation potential of canine induced pluripotent stem cells.

Toshiya Nishimura, Kazuto Kimura, Kyomi J Igarashi, Kohei Shishida, Hiroko Sugisaki, Masaya Tsukamoto, Aadhavan Balakumar, Chihiro Funamoto, Masumi Hirabayashi, Amir Kol and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
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.

Toshiya NishimuraPremium Research Institute for Human Metaverse Medicine (WPI-PRIMe), The University of Osaka, Suita, Osaka 565-0871, Japan. Electronic address: tnishimu.kbb@osaka-u.ac.jp.
Kazuto KimuraDepartment of Advanced Pathobiology, Graduate School of Veterinary Sciences, Osaka Metropolitan University, Izumisano, Osaka 598-8531, Japan; Department of Pathology, Microbiology & Immunology, School of Veterinary Medicine, University of California, Davis, Davis, CA 95616, USA.
Kyomi J IgarashiInstitute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA; Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
Kohei ShishidaDepartment of Advanced Pathobiology, Graduate School of Veterinary Sciences, Osaka Metropolitan University, Izumisano, Osaka 598-8531, Japan.
Hiroko SugisakiDepartment of Advanced Pathobiology, Graduate School of Veterinary Sciences, Osaka Metropolitan University, Izumisano, Osaka 598-8531, Japan.
Masaya TsukamotoDepartment of Advanced Pathobiology, Graduate School of Veterinary Sciences, Osaka Metropolitan University, Izumisano, Osaka 598-8531, Japan.
Aadhavan BalakumarDepartment of Pathology, Microbiology & Immunology, School of Veterinary Medicine, University of California, Davis, Davis, CA 95616, USA.
Chihiro FunamotoDivision of Stem Cell and Organoid Medicine, Department of Genome Biology, Graduate School of Medicine, The University of Osaka, Osaka 565-0871, Japan.
Masumi HirabayashiCenter for Genetic Analysis of Behavior, National Institute for Physiological Sciences, Okazaki, Aichi 444-8787, Japan; The Graduate University of Advanced Studies, Okazaki, Aichi 444-8787, Japan.
Amir KolDepartment of Pathology, Microbiology & Immunology, School of Veterinary Medicine, University of California, Davis, Davis, CA 95616, USA.
Shingo HatoyaDepartment of Advanced Pathobiology, Graduate School of Veterinary Sciences, Osaka Metropolitan University, Izumisano, Osaka 598-8531, Japan. Electronic address: hatoya@omu.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Naturally occurring diseases in companion dogs are increasingly being recognized as valuable translational disease models. While induced pluripotent stem cell (iPSC) technology had revolutionized the field of human bio-medical research, canine iPSC (ciPSC) technology is still in its infancy, and robust canine-specific iPSC medium formulations and differentiation protocols are lacking. Here, we have established NANOG-reporter ciPSC lines and found that fibroblast growth factor (FGF), activin/transforming growth factor (TGF)-β, and WNT signals were critical for the robust maintenance of ciPSCs. Manipulating these signaling pathways stabilized the culture of ciPSC regardless of the cell line or basal medium. ciPSCs cultured in the optimized medium showed a homogenized global gene expression pattern. Furthermore, the ciPSCs cultured in this medium successfully differentiated into cardiomyocytes displaying homogenous contraction as well as sarcomere alignment. This robust culture condition provides a valuable resource to facilitate the utilization of ciPSCs for various studies, including human disease modeling.

Indexed as

Cell Culture TechniquesCell DifferentiationInduced Pluripotent Stem CellsSignal TransductionActivinsAnimalsCell LineCulture MediaDogsFibroblast Growth FactorsHumansMyocytes, CardiacTransforming Growth Factor betaActivinsCulture MediaFibroblast Growth FactorsTransforming Growth Factor betaanimalcaninecardiomyocytegene editinginduced pluripotent stem cellsprimed pluripotent stem cellsreporter line

Identifiers

PMID40972586
PMCPMC12790732

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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.