Evidence map›Paper›PMID 40341813›Full record

ArticleCommunications biology2025

TRPV2 mediates stress resilience in mouse cardiomyocytes.

Yubing Dong, Guohao Wang, Yoshihiro Ujihara, Yanzhu Chen, Masashi Yoshida, Kazufumi Nakamura, Kimiaki Katanosaka, Keiji Naruse, Yuki Katanosaka

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Lysophosphatidylcholine sensitizes TRPV2 by indirect mechanisms.Pflugers Archiv : European journal of physiology · 2025
    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

9 authors.

Yubing DongDepartment of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
Guohao WangDepartment of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
Yoshihiro UjiharaDepartment of Electrical and Mechanical Engineering, Graduate School of Engineering, Nagoya Institute of Technology, Nagoya, Aichi, Japan.
Yanzhu ChenDepartment of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
Masashi YoshidaDepartment of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Kazufumi NakamuraDepartment of Cardiovascular Medicine, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.ORCID http://orcid.org/0000-0001-8845-3626
Kimiaki KatanosakaDepartment of Biomedical Sciences, College of Life and Health Sciences, Chubu University, Kasugai, Aichi, Japan.
Keiji NaruseDepartment of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.ORCID http://orcid.org/0000-0003-4100-6444
Yuki KatanosakaDepartment of Cardiovascular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan. katanosaka@kinjo-u.ac.jp.ORCID http://orcid.org/0000-0002-0250-4312

Funding

Ministry of Education, Culture, Sports, Science and Technology (MEXT) 23722363
6 · The paper itself

Abstract

The heart dynamically compensates for haemodynamic stress, but how this resilience forms during cardiac growth is not clear. Using a temporally inducible, cardiac-specific knockout in mice we show that the Transient receptor potential vanilloid family 2 (TRPV2) channel is crucial for the maturation of cardiomyocyte stress resilience. TRPV2 defects in growing hearts lead to small morphology, abnormal intercalated discs, weak contractility, and low expression of serum response factor and Insulin-like growth factor-1 (IGF-1) signalling. Individual cardiomyocytes of TRPV2-deficient hearts show reduced contractility with abnormal Ca

Indexed as

Calcium ChannelsMyocytes, CardiacStress, PhysiologicalTRPV Cation ChannelsAnimalsCalciumCells, CulturedInsulin-Like Growth Factor IMiceMice, KnockoutMyocardial ContractionCalciumCalcium ChannelsInsulin-Like Growth Factor ITrpv2 protein, mouseTRPV Cation Channels

Identifiers

PMID40341813
PMCPMC12062233

What Socratic 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 Socratic graph.