Evidence map›Paper›PMID 40934809›Full record

ArticleJACC. Basic to translational science2025

Integrative Transcriptomic-Histological Analysis in Dilated Cardiomyopathy Unveils FGFR1 Inhibition as Anti-Cardiac Fibrotic and Cardioprotective Therapy.

Reo Hata, Shunsuke Funakoshi, Takeru Makiyama, Takao Kato, Megumi Narita, Yasuko Matsumura, Ryoko Hirohata, Yuki Naka, Kazumi Ida, Hiroaki Ito and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in JACC. Basic to translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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. Pillars of Peer Review.JACC. Basic to translational science · 2026
    Article
  2. 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

17 authors.

Reo HataDepartment of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto, Japan; Department of Cell Growth and Differentiation, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan.
Shunsuke FunakoshiDepartment of Cell Growth and Differentiation, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan; Takeda-CiRA Joint Program, Kanagawa, Japan. Electronic address: s.funakoshi@cira.kyoto-u.ac.jp.
Takeru MakiyamaDepartment of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto, Japan.
Takao KatoDepartment of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto, Japan.
Megumi NaritaDepartment of Cell Growth and Differentiation, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan.
Yasuko MatsumuraDepartment of Cell Growth and Differentiation, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan.
Ryoko HirohataDepartment of Cell Growth and Differentiation, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan.
Yuki NakaDepartment of Cell Growth and Differentiation, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan; Takeda-CiRA Joint Program, Kanagawa, Japan.
Kazumi IdaDepartment of Cell Growth and Differentiation, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan; Takeda-CiRA Joint Program, Kanagawa, Japan.
Hiroaki ItoDepartment of Diagnostic Pathology, Kyoto University Hospital, Sakyo-ku, Kyoto, Japan.
Akihiko YoshizawaDepartment of Diagnostic Pathology, Kyoto University Hospital, Sakyo-ku, Kyoto, Japan; Department of Diagnostic Pathology, Nara Medical University, Nara, Japan.
Yasuhito NannyaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto, Japan; Department of Hematology and Oncology, Tokyo University Medical Research Institute, Tokyo, Japan.
Hironori HagaDepartment of Diagnostic Pathology, Kyoto University Hospital, Sakyo-ku, Kyoto, Japan.
Seishi OgawaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto, Japan; Institute for the Advanced Study of Human Biology (WPI-ASHBi), Kyoto University, Sakyo-ku, Kyoto, Japan.
Koh OnoDepartment of Cardiovascular Medicine, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto, Japan.
Takeshi KimuraDepartment of Cardiology, Hirakata Kosai Hospital, Hirakata-city, Osaka, Japan.
Yoshinori YoshidaDepartment of Cell Growth and Differentiation, Center for iPS Cell Research and Application (CiRA), Kyoto University, Sakyo-ku, Kyoto, Japan; Takeda-CiRA Joint Program, Kanagawa, Japan. Electronic address: yoshinor@cira.kyoto-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac fibrosis drives dysfunction in dilated cardiomyopathy (DCM); yet, effective therapies are limited. This study identifies FGFR1 as a critical target in cardiac fibrosis using transcriptomic and histological analyses of 58 human DCM biopsies. FGFR1 expression correlated with fibrosis severity, and inhibition by AZD4547 reduced fibrosis and improved cardiac function in organoid and murine models. These findings validate FGFR1 inhibition as a promising therapeutic strategy for mitigating fibrosis and improving outcomes in heart failure associated with DCM.

Indexed as

cardiac fibrosiscardiac fibrosis organoid modeldilated cardiomyopathyFGFR inhibitiontranscriptomics

Identifiers

PMID40934809
PMCPMC12665400

What OpenQuestion holds

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LicenceCC BY-NC-ND
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 OpenQuestion graph.