Evidence map›Paper›PMID 35731090›Full record

ArticleeLife2022

Activation of transient receptor potential vanilloid 4 is involved in pressure overload-induced cardiac hypertrophy.

Yan Zou, Miaomiao Zhang, Qiongfeng Wu, Ning Zhao, Minwei Chen, Cui Yang, Yimei Du, Bing Han

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

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  12. Imaging methods to monitor and quantify cell differentiation.Frontiers in cell and developmental biology · 2025
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  19. Ubiquitin-specific protease 38 promotes inflammatory atrial fibrillation induced by pressure overload.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2023
    Article
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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

8 authors at 3 institutions in 1 country.

Yan Zou *Department of Cardiology, Xuzhou Central Hospital, Xuzhou, China.
Miaomiao Zhang *Department of Cardiology, Xuzhou Central Hospital, Xuzhou, China.
Qiongfeng WuDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ning ZhaoDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Minwei ChenDepartment of Cardiology, Xiamen Key Laboratory of Cardiac Electrophysiology, Xiamen Institute of Cardiovascular Diseases, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
Cui YangDepartment of Cardiology, Xiamen Key Laboratory of Cardiac Electrophysiology, Xiamen Institute of Cardiovascular Diseases, The First Affiliated Hospital of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
Yimei DuDepartment of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.ORCID 0000-0003-1125-0294
Bing HanDepartment of Cardiology, Xuzhou Central Hospital, Xuzhou, China.
Huazhong University of Science and Technology · CNXuzhou Central Hospital · CNFirst Affiliated Hospital of Xiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies, including our own, have demonstrated that transient receptor potential vanilloid 4 (TRPV4) is expressed in hearts and implicated in cardiac remodeling and dysfunction. However, the effects of TRPV4 on pressure overload-induced cardiac hypertrophy remain unclear. In this study, we found that TRPV4 expression was significantly increased in mouse hypertrophic hearts, human failing hearts, and neurohormone-induced hypertrophic cardiomyocytes. Deletion of TRPV4 attenuated transverse aortic constriction (TAC)-induced cardiac hypertrophy, cardiac dysfunction, fibrosis, inflammation, and the activation of NFκB - NOD - like receptor pyrin domain-containing protein 3 (NLRP3) in mice. Furthermore, the TRPV4 antagonist GSK2193874 (GSK3874) inhibited cardiac remodeling and dysfunction induced by TAC. In vitro, pretreatment with GSK3874 reduced the neurohormone-induced cardiomyocyte hypertrophy and intracellular Ca

Indexed as

Calcium-Calmodulin-Dependent Protein Kinase Type 2Ventricular RemodelingAnimalsCardiomegalyMiceMice, Inbred C57BLMice, Inbred NODMyocytes, CardiacNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinTRPV Cation ChannelsCalcium-Calmodulin-Dependent Protein Kinase Type 2NF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinTrpv4 protein, mouseTRPV Cation Channelsca2+/calmodulin-dependent protein kinase iicardiac hypertrophycell biologymouseTRPV4

Identifiers

PMID35731090
PMCPMC9224988
OpenAlexW4283260401

What OpenQuestion holds

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LicenceCC BY
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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.