Evidence map›Paper›PMID 37456848›Full record

ArticleiScience2023

Wnt5a-YAP signaling axis mediates mechanotransduction in cardiac myocytes and contributes to contractile dysfunction induced by pressure overload.

Hiroshi Kishimoto, Masayoshi Iwasaki, Kensaku Wada, Keita Horitani, Osamu Tsukamoto, Kenta Kamikubo, Seitaro Nomura, Shinji Matsumoto, Takeshi Harada, Daisuke Motooka and 5 more

Open access · goldAbstract read
In one paragraph

Article in iScience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
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  5. Review
  6. Wnt signaling in cardiac development and heart diseases.In vitro cellular & developmental biology. Animal · 2024
    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 at 4 institutions in 1 country.

Hiroshi KishimotoDepartment of Medicine II, Kansai Medical University, Osaka 573-1010, Japan.
Masayoshi IwasakiDepartment of Medicine II, Kansai Medical University, Osaka 573-1010, Japan.
Kensaku WadaDepartment of Medicine II, Kansai Medical University, Osaka 573-1010, Japan.
Keita HoritaniDepartment of Medicine II, Kansai Medical University, Osaka 573-1010, Japan.
Osamu TsukamotoDepartment of Medical Biochemistry, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan.
Kenta KamikuboDepartment of Medical Biochemistry, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan.
Seitaro NomuraDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Shinji MatsumotoDepartment of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan.
Takeshi HaradaDepartment of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan.
Daisuke MotookaGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan.
Daisuke OkuzakiGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan.
Seiji TakashimaDepartment of Medical Biochemistry, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan.
Issei KomuroDepartment of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Akira KikuchiDepartment of Molecular Biology and Biochemistry, Osaka University Graduate School of Medicine, Osaka 565-0871, Japan.
Ichiro ShiojimaDepartment of Medicine II, Kansai Medical University, Osaka 573-1010, Japan.
Osaka University · JPKansai Medical University · JPThe University of Tokyo · JPOsaka Medical Center for Cancer and Cardiovascular Diseases · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-canonical Wnt signaling activated by Wnt5a/Wnt11 is required for the second heart field development in mice. However, the pathophysiological role of non-canonical Wnt signaling in the adult heart has not been fully elucidated. Here we show that cardiomyocyte-specific

Indexed as

Cardiovascular medicineMolecular physiology

Identifiers

PMID37456848
PMCPMC10338234
OpenAlexW4380987519

What OpenQuestion holds

Textmetadata
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.