Evidence map›Paper›PMID 29292365›Full record

ArticleAnnals of transplantation2018

Antifibrotic Effects of Hepatocyte Growth Factor on Endothelial-to-Mesenchymal Transition via Transforming Growth Factor-Beta1 (TGF-β1)/Smad and Akt/mTOR/P70S6K Signaling Pathways.

Zijie Wang, Shuang Fei, Chuanjian Suo, Zhijian Han, Jun Tao, Zhen Xu, Chunchun Zhao, Ruoyun Tan, Min Gu

Open access · hybridAbstract read
In one paragraph

Article in Annals of transplantation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Zijie WangDepartment of Urology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China (mainland).
Shuang FeiDepartment of Urology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China (mainland).
Chuanjian SuoDepartment of Urology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China (mainland).
Zhijian HanDepartment of Urology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China (mainland).
Jun TaoDepartment of Urology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China (mainland).
Zhen XuDepartment of Urology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China (mainland).
Chunchun ZhaoDepartment of Urology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China (mainland).
Ruoyun TanDepartment of Urology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China (mainland).
Min GuDepartment of Urology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu, China (mainland).
Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND The related mechanisms involved in allograft interstitial fibrosis and chronic allograft dysfunction (CAD), following renal transplant, remain largely unknown. Here, we explored the role of hepatocyte growth factor (HGF) treatment on the endothelial-to-mesenchymal transition (EndMT) as a new way to target and prevent kidney fibrosis and improve outcomes for renal transplant recipients. MATERIAL AND METHODS We extracted proteins and mRNAs from human umbilical vein endothelial cells (HUVECs) and human renal glomerular endothelial cells (HRGECs) treated with transforming growth factor-beta1 (TGF-β1) and/or varying doses of HGF, and assessed the effect of HGF on the EndMT using western blotting, qRT-PCR, and ELISA assays. We utilized cell motility and migration assays to evaluate cell movement, and applied western blotting to assess the mechanism by which TGF-β1 induced the EndMT. RESULTS HGF significantly attenuated the development of TGF-β1-induced EndMT in a concentration-dependent way, and weakened the abilities of motility and migration of both HUVECs and HRGECs. Moreover, our results reveal that the antifibrotic effect of HGF on the EndMT was associated with the TGF-β/Smad and Akt/mTOR/p70S6K signaling pathways. CONCLUSIONS Our study suggests that HGF treatment significantly attenuates the development of EndMT induced by TGF-β1 via the TGFb/Smad and Akt/mTOR/P70S6K signaling, which provides novel insights into the prevention and treatment of interstitial fibrosis and CAD following renal transplant.

Indexed as

Cell MovementHepatocyte Growth FactorHumansHuman Umbilical Vein Endothelial CellsProto-Oncogene Proteins c-aktRibosomal Protein S6 Kinases, 70-kDaSignal TransductionTOR Serine-Threonine KinasesTransforming Growth Factor beta1Wound HealingHepatocyte Growth FactorProto-Oncogene Proteins c-aktRibosomal Protein S6 Kinases, 70-kDaTOR Serine-Threonine KinasesTransforming Growth Factor beta1

Identifiers

PMID29292365
PMCPMC6248046
OpenAlexW2782422152

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.