Evidence map›Paper›PMID 24840640›Full record

ArticleInternational journal of molecular medicine2014

Hepatocyte growth factor regulates the TGF-β1-induced proliferation, differentiation and secretory function of cardiac fibroblasts.

Xin Yi, Xiaoyan Li, Yanli Zhou, Shan Ren, Weiguo Wan, Gaoke Feng, Xuejun Jiang

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.9field-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

35 citing papers in PubMed, 57 citations in OpenAlex.

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  20. The Role of the TGF-β Superfamily in Myocardial Infarction.Frontiers in cardiovascular medicine · 2019
    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

7 authors at 2 institutions in 1 country.

Xin YiDepartment of Cardiology, Renmin Hospital of Wuhan University and Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Xiaoyan LiDepartment of Cardiology, Renmin Hospital of Wuhan University and Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Yanli ZhouDepartment of Cardiology, Renmin Hospital of Wuhan University and Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Shan RenDepartment of Cardiology, Renmin Hospital of Wuhan University and Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Weiguo WanDepartment of Cardiology, Renmin Hospital of Wuhan University and Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Gaoke FengDepartment of Cardiology, Renmin Hospital of Wuhan University and Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Xuejun JiangDepartment of Cardiology, Renmin Hospital of Wuhan University and Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.
Renmin Hospital of Wuhan University · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac fibroblast (CF) proliferation and transformation into myofibroblasts play important roles in cardiac fibrosis during pathological myocardial remodeling. In this study, we demonstrate that hepatocyte growth factor (HGF), an antifibrotic factor in the process of pulmonary, renal and liver fibrosis, is a negative regulator of cardiac fibroblast transformation in response to transforming growth factor‑β1 (TGF‑β1). HGF expression levels were significantly reduced in the CFs following treatment with 5 ng/ml TGF‑β1 for 48 h. The overexpression of HGF suppressed the proliferation, transformation and the secretory function of the CFs following treatment with TGF‑β1, as indicated by the attenuated expression levels of α-smooth muscle actin (α‑SMA) and collagen I and III, whereas the knockdown of HGF had the opposite effect. Mechanistically, we identified that the phosphorylation of c‑Met, Akt and total protein of TGIF was significantly inhibited by the knockdown of HGF, but was significantly enhanced by HGF overexpression. Collectively, these results indicate that HGF activates the c‑Met‑Akt‑TGIF signaling pathway, inhibiting CF proliferation and transformation in response to TGF‑β1 stimulation.

Indexed as

AnimalsCell DifferentiationCell ProliferationGene Expression RegulationGene Knockdown TechniquesHeart FailureHepatocyte Growth FactorHumansMyofibroblastsOncogene Protein v-aktProto-Oncogene Proteins c-metRatsSignal TransductionTransforming Growth Factor beta1Hepatocyte Growth FactorOncogene Protein v-aktProto-Oncogene Proteins c-metTransforming Growth Factor beta1

Identifiers

PMID24840640
PMCPMC4094591
OpenAlexW2076442890

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.