Evidence map›Paper›PMID 39266515›Full record

ArticleNature communications2024

Protein kinase N promotes cardiac fibrosis in heart failure by fibroblast-to-myofibroblast conversion.

Satoya Yoshida, Tatsuya Yoshida, Kohei Inukai, Katsuhiro Kato, Yoshimitsu Yura, Tomoki Hattori, Atsushi Enomoto, Koji Ohashi, Takahiro Okumura, Noriyuki Ouchi and 5 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. TRIM40 Drives Pathological Cardiac Hypertrophy and Heart Failure via Ubiquitination of PKN2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  9. Review
  10. Article
  11. The pathophysiological role of MiRNAs in heart failure.Frontiers in cardiovascular medicine · 2026
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Long noncoding RNA MEG3: an active player in fibrosis.Pharmacological reports : PR · 2025
    Review
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.

Satoya YoshidaDepartment of Cardiology, Nagoya University School of Medicine, Nagoya, Japan.
Tatsuya YoshidaDepartment of Cardiology, Nagoya University School of Medicine, Nagoya, Japan.ORCID 0000-0003-0364-4680
Kohei InukaiDepartment of Cardiology, Nagoya University School of Medicine, Nagoya, Japan.
Katsuhiro KatoDepartment of Cardiology, Nagoya University School of Medicine, Nagoya, Japan.ORCID 0000-0002-9710-1451
Yoshimitsu YuraDepartment of Cardiology, Nagoya University School of Medicine, Nagoya, Japan.
Tomoki HattoriDepartment of Cardiology, Nagoya University School of Medicine, Nagoya, Japan.
Atsushi EnomotoDepartment of Pathology, Nagoya University School of Medicine, Nagoya, Japan.ORCID 0000-0002-9206-6116
Koji OhashiDepartment of Molecular Medicine and Cardiology, Nagoya University School of Medicine, Nagoya, Japan.ORCID 0000-0002-9666-026X
Takahiro OkumuraDepartment of Cardiology, Nagoya University School of Medicine, Nagoya, Japan.ORCID 0000-0001-5076-2052
Noriyuki OuchiDepartment of Molecular Medicine and Cardiology, Nagoya University School of Medicine, Nagoya, Japan.ORCID 0009-0003-8598-3498
Haruya KawaseDepartment of Cardiology, Nagoya University School of Medicine, Nagoya, Japan.ORCID 0000-0002-8927-0896
Nina WettschureckDepartment of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.ORCID 0000-0001-6858-1460
Stefan OffermannsDepartment of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.ORCID 0000-0001-8676-6805
Toyoaki MuroharaDepartment of Cardiology, Nagoya University School of Medicine, Nagoya, Japan.ORCID 0000-0003-2723-6243
Mikito TakefujiDepartment of Cardiology, Nagoya University School of Medicine, Nagoya, Japan. takefuji@med.nagoya-u.ac.jp.ORCID 0000-0003-4870-7913

Funding

Japan Science Society 23H02903
6 · The paper itself

Abstract

Chronic fibrotic tissue disrupts various organ functions. Despite significant advances in therapies, mortality and morbidity due to heart failure remain high, resulting in poor quality of life. Beyond the cardiomyocyte-centric view of heart failure, it is now accepted that alterations in the interstitial extracellular matrix (ECM) also play a major role in the development of heart failure. Here, we show that protein kinase N (PKN) is expressed in cardiac fibroblasts. Furthermore, PKN mediates the conversion of fibroblasts into myofibroblasts, which plays a central role in secreting large amounts of ECM proteins via p38 phosphorylation signaling. Fibroblast-specific deletion of PKN led to a reduction of myocardial fibrotic changes and cardiac dysfunction in mice models of ischemia-reperfusion or heart failure with preserved ejection fraction. Our results indicate that PKN is a therapeutic target for cardiac fibrosis in heart failure.

Indexed as

FibroblastsFibrosisHeart FailureMyocardiumMyofibroblastsProtein Kinase CAnimalsDisease Models, AnimalExtracellular MatrixHumansMaleMiceMice, Inbred C57BLMice, Knockoutp38 Mitogen-Activated Protein KinasesPhosphorylationp38 Mitogen-Activated Protein KinasesProtein Kinase Cprotein kinase N

Identifiers

PMID39266515
PMCPMC11392935

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LicenceCC BY-NC-ND
Read underepoch 390

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.