Evidence map›Paper›PMID 26198166›Full record

ArticleStem cells translational medicine2015

Cell Therapy Using Human Induced Pluripotent Stem Cell-Derived Renal Progenitors Ameliorates Acute Kidney Injury in Mice.

Takafumi Toyohara, Shin-Ichi Mae, Shin-Ichi Sueta, Tatsuyuki Inoue, Yukiko Yamagishi, Tatsuya Kawamoto, Tomoko Kasahara, Azusa Hoshina, Taro Toyoda, Hiromi Tanaka and 8 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cells translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
7.8field-weighted citation impact, top 2% of its field
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

77 citing papers in PubMed, 154 citations in OpenAlex.

  1. Review
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  12. Induced pluripotent stem cell-based therapies for organ fibrosis.Frontiers in bioengineering and biotechnology · 2023
    Review
  13. Review
  14. Development of Cell Therapies for Renal Disease and Regenerative Medicine.International journal of molecular sciences · 2022
    Review
  15. Article
  16. Article
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  18. Physiology assays in human kidney organoids.American journal of physiology. Renal physiology · 2022
    Review
  19. Article
  20. Article

17 more citing papers are in PubMed but not listed here.

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

18 authors at 4 institutions in 2 countries.

Takafumi ToyoharaCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Shin-Ichi MaeCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Shin-Ichi SuetaCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Tatsuyuki InoueCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Yukiko YamagishiCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Tatsuya KawamotoCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Tomoko KasaharaCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Azusa HoshinaCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Taro ToyodaCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Hiromi TanakaCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Toshikazu AraokaCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Aiko Sato-OtsuboCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Kazutoshi TakahashiCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Yasunori SatoCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Noboru YamajiCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Seishi OgawaCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Shinya YamanakaCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA.
Kenji OsafuneCenter for iPS Cell Research and Application (CiRA), Kyoto University, Kyoto, Japan; Drug Discovery Research, Astellas Pharma Inc., Ibaraki, Japan; Department of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan; Clinical Research Center, Chiba University of Medicine, Chiba, Japan; Gladstone Institute of Cardiovascular Disease, San Francisco, California, USA osafu@cira.kyoto-u.ac.jp.
Kyoto University · JPAstellas Pharma (Japan) · JPChiba University · JPGladstone Institutes · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledAcute kidney injury (AKI) is defined as a rapid loss of renal function resulting from various etiologies, with a mortality rate exceeding 60% among intensive care patients. Because conventional treatments have failed to alleviate this condition, the development of regenerative therapies using human induced pluripotent stem cells (hiPSCs) presents a promising new therapeutic option for AKI. We describe our methodology for generating renal progenitors from hiPSCs that show potential in ameliorating AKI. We established a multistep differentiation protocol for inducing hiPSCs into OSR1+SIX2+ renal progenitors capable of reconstituting three-dimensional proximal renal tubule-like structures in vitro and in vivo. Moreover, we found that renal subcapsular transplantation of hiPSC-derived renal progenitors ameliorated the AKI in mice induced by ischemia/reperfusion injury, significantly suppressing the elevation of blood urea nitrogen and serum creatinine levels and attenuating histopathological changes, such as tubular necrosis, tubule dilatation with casts, and interstitial fibrosis. To our knowledge, few reports demonstrating the therapeutic efficacy of cell therapy with renal lineage cells generated from hiPSCs have been published. Our results suggest that regenerative medicine strategies for kidney diseases could be developed using hiPSC-derived renal cells. SIGNIFICANCE: This report is the first to demonstrate that the transplantation of renal progenitor cells differentiated from human induced pluripotent stem (iPS) cells has therapeutic effectiveness in mouse models of acute kidney injury induced by ischemia/reperfusion injury. In addition, this report clearly demonstrates that the therapeutic benefits come from trophic effects by the renal progenitor cells, and it identifies the renoprotective factors secreted by the progenitors. The results of this study indicate the feasibility of developing regenerative medicine strategy using iPS cells against renal diseases.

Indexed as

Acute Kidney InjuryAnimalsBiomarkersBlood Urea NitrogenCell- and Tissue-Based TherapyCell DifferentiationCells, CulturedCreatinineEpithelial CellsFibrosisGene ExpressionHomeodomain ProteinsHumansInduced Pluripotent Stem CellsKidney TubulesMaleBiomarkersCreatinineHomeodomain ProteinsNerve Tissue ProteinsOSR1 protein, humanSIX2 protein, humanTranscription FactorsAcute kidney injuryCell- and tissue-based therapyInduced pluripotent stem cellsKidneyNephronsRenal progenitorsSIX2 protein

Identifiers

PMID26198166
PMCPMC4542865
OpenAlexW2114698242

What OpenQuestion holds

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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.