Evidence map›Paper›PMID 41953004›Full record

ArticleiScience2026

Human iPSC cardiomyocyte patch transplantation modifies extracellular matrix and fibroblast behavior after myocardial infarction.

Kosuke Torigata, Ryohei Matsuura, Fumiya Nagatomo, Moe Thiha, Takao Hikita, Hiroko Iseoka, Hiromitsu Takagi, Uichi Koshimizu, Hiroki Sakakima, Satoshi Izumi and 5 more

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Article in iScience, 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

15 authors.

Kosuke TorigataCuorips Inc., Tokyo, Japan.
Ryohei MatsuuraMax Planck Institute for Heart and Lung Research, Laboratory for Cell Polarity and Organogenesis, Bad Nauheim, Germany.
Fumiya NagatomoDepartment of Mechanical Engineering, School of Engineering, The University of Tokyo, Tokyo, Japan.
Moe ThihaDepartment of Pathophysiology and Drug Discovery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Okayama University, Okayama, Japan.
Takao HikitaMax Planck Institute for Heart and Lung Research, Laboratory for Cell Polarity and Organogenesis, Bad Nauheim, Germany.
Hiroko IseokaDepartment of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Hiromitsu TakagiDaiichi Sankyo Co., Ltd., Tokyo, Japan.
Uichi KoshimizuDaiichi Sankyo Co., Ltd., Tokyo, Japan.
Hiroki SakakimaDepartment of Mechanical Engineering, School of Engineering, The University of Tokyo, Tokyo, Japan.
Satoshi IzumiDepartment of Mechanical Engineering, School of Engineering, The University of Tokyo, Tokyo, Japan.
Asuka HatanoDepartment of Mechanical Engineering, School of Engineering, The University of Tokyo, Tokyo, Japan.
Thomas BraunMaxPlanck Institute for Heart and Lung Research, Department of Cardiac Development and Remodeling, Bad Nauheim, Germany.
Yoshiki SawaDepartment of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Shigeru MiyagawaDepartment of Cardiovascular Surgery, Osaka University Graduate School of Medicine, Osaka, Japan.
Masanori NakayamaMax Planck Institute for Heart and Lung Research, Laboratory for Cell Polarity and Organogenesis, Bad Nauheim, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial infarction (MI) followed by chronic heart failure is the main cause of mortality of heart diseases. Although reparative cell transplantation therapies with pluripotent stem cell-derived cardiomyocytes (CMs) represent a promising therapeutic strategy, molecular mechanisms of the therapy remain elusive. Here, we show that transplantation of the human induced pluripotent stem cell (hiPSC)-derived CM patch onto the damaged heart after MI increases the ratio of collagen type I against collagen type III to modulate alignment of the collagen fibers at the infarcted zone. As a result, tissue elasticity of the heart is improved, and fibrosis at the remote zone is reduced. Mechanistically, we find that hiPSC-derived CM patches secrete TGF-β1, directly inducing collagen type I production in fibroblasts but not collagen type III. Our results suggest the direct effect of the transplanted CM patch on the cardiac fibroblasts to improve elasticity of the damaged heart, resulting in functional recovery after MI.

Indexed as

cell biologyfibrosisstem cell research

Identifiers

PMID41953004
PMCPMC13053790

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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.