Evidence map›Paper›PMID 32329036›Full record

ArticleCardiology journal2020

Transient receptor potential channel TRPV4 mediates TGF-β1-induced differentiation of human ventricular fibroblasts.

Min-Soo Ahn, Young Woo Eom, Ji-Eun Oh, Seung-Kuy Cha, Kyu Sang Park, Jung-Woo Son, Jun-Won Lee, Young Jin Youn, Sung Gyun Ahn, Jang-Young Kim and 3 more

Abstract read
In one paragraph

Article in Cardiology journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

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  10. CaBiomedicines · 2025
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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

13 authors.

Min-Soo AhnCardiology Division, Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea, Republic Of.
Young Woo EomCell Therapy and Tissue Engineering Center, Yonsei University Wonju College of Medicine, Wonju, Korea, Republic Of.
Ji-Eun OhCell Therapy and Tissue Engineering Center, Yonsei University Wonju College of Medicine, Wonju, Korea, Republic Of.
Seung-Kuy ChaDepartment of Physiology, Yonsei University Wonju College of Medicine, Wonju, Korea, Republic Of.
Kyu Sang ParkDepartment of Physiology, Yonsei University Wonju College of Medicine, Wonju, Korea, Republic Of.
Jung-Woo SonCardiology Division, Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea, Republic Of.
Jun-Won LeeCardiology Division, Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea, Republic Of.
Young Jin YounCardiology Division, Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea, Republic Of.
Sung Gyun AhnCardiology Division, Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea, Republic Of.
Jang-Young KimCardiology Division, Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea, Republic Of.
Seung-Hwan LeeCardiology Division, Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea, Republic Of.
Junghan YoonCardiology Division, Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea, Republic Of.
Byung-Su YooCardiology Division, Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea, Republic Of. yubs@yonsei.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiac fibroblasts (CFs) are principal extracellular matrix-producing cells. In response to injury, CFs transdifferentiate into myofibroblasts. Intracellular calcium (Ca2+) signaling, involved in fibroblast proliferation and differentiation, is activated in fibroblasts through transient receptor potential (TRP) channels, but the function of these channels has not been investigated in human ventricular CFs. Under evaluation in this study, was the role of TRP channels in the differentiation of human ventricular CFs induced by transforming the growth factor beta (TGF-β), a pro-fibrotic cytokine.

methodsHuman ventricular CFs were used in this study. The differentiation of CFs into myofibroblast was induced with TGF-β and was identified by the expression of smooth muscle actin.

resultsResults indicate that Ca2+ signaling was an essential component of ventricular CF dif-ferentiation. CFs treated with TGF-β demonstrated increased expression of a TRP channel, TRPV4, both at the mRNA and protein levels, which corresponded with CF-myofibroblast trans-differentiation, as evidenced by the upregulation of α-smooth muscle actin, a myofibroblast marker, and plasminogen activator inhibitor-1, which are fibrogenesis markers. An agonist of TRPV4 induced the conversion of CFs into myofibroblasts, whereas it's antagonist as well a Ca2+ chelating agent reduced it, indicating that the Ca2+ influx throughTRPV4 is required for CF trans-differentiation. Overall, these results dem-onstrate that TRPV4-mediated Ca2+ influx participates in regulating the differentiation of human ventricular CFs into myofibroblasts through the MAPK/ERK pathway.

conclusionsOverall, these results demonstrate that TRPV4-mediated Ca2+ influx participates in regulating the differentiation of human ventricular CFs into myofibroblasts through the MAPK/ERK pathway.

Indexed as

ActinsCalcium SignalingCells, CulturedCell TransdifferentiationExtracellular Signal-Regulated MAP KinasesHeart VentriclesHumansMyofibroblastsTransforming Growth Factor beta1TRPV Cation ChannelsActinsExtracellular Signal-Regulated MAP KinasesTGFB1 protein, humanTransforming Growth Factor beta1TRPV4 protein, humanTRPV Cation Channelscalciumfibroblastmyofibroblasttransient receptor potential channels

Identifiers

PMID32329036
PMCPMC8016025

What OpenQuestion holds

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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.