Evidence map›Paper›PMID 27602565›Full record

ArticlePloS one2016

GSTA3 Attenuates Renal Interstitial Fibrosis by Inhibiting TGF-Beta-Induced Tubular Epithelial-Mesenchymal Transition and Fibronectin Expression.

Yun Xiao, Jishi Liu, Yu Peng, Xuan Xiong, Ling Huang, Huixiang Yang, Jian Zhang, Lijian Tao

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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

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

  1. Pooled it
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  9. Review
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  13. GSTA3 regulates TGF-The Journal of international medical research · 2019
    Article
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  18. Restoration of renal hemodynamics and functions byInternational journal of health sciences
    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

8 authors at 4 institutions in 2 countries.

Yun XiaoDivision of Nephrology, Xiangya Hospital, Central South University, Changsha, China, 410078.
Jishi LiuDivision of Nephrology, Xiangya Hospital, Central South University, Changsha, China, 410078.
Yu PengDivision of Nephrology, Xiangya Hospital, Central South University, Changsha, China, 410078.
Xuan XiongDivision of Nephrology, Xiangya Hospital, Central South University, Changsha, China, 410078.
Ling HuangDivision of Nephrology, Xiangya Hospital, Central South University, Changsha, China, 410078.
Huixiang YangDivision of Digestive Medicine, Xiangya Hospital, Central South University, Changsha, China, 410078.
Jian ZhangDepartment of Microbial Infection and Immunity, The Ohio State University, Columbus, Ohio, United States of America.
Lijian TaoDivision of Nephrology, Xiangya Hospital, Central South University, Changsha, China, 410078.
Central South University · CNXiangya Hospital Central South University · CNGuangzhou Medical University · CNThe Ohio State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tubular epithelial-mesenchymal transition (EMT) has been widely accepted as the underlying mechanisms of renal interstitial fibrosis (RIF). The production of reactive oxygen species (ROS) plays a vital role in tubular EMT process. The purpose of this study was to investigate the involved molecular mechanisms in TGF-beta-induced EMT and identify the potential role of glutathione S-transferase alpha 3 (GSTA3) in this process. The iTRAQ screening was performed to identify protein alterations of the rats underwent unilateral-ureteral obstruction (UUO). Protein expression of GSTA3 in patients with obstructive nephropathy and UUO rats was detected by immunohistochemistry. Protein and mRNA expression of GSTA3 in UUO rats and NRK-52E cells were determined by Western blot and RT-PCR. siRNA and overexpression plasmid were transfected specifically to assess the role of GSTA3 in RIF. The generation of ROS was measured by dichlorofluorescein fluorescence analysis. GSTA3 protein and mRNA expression was significantly reduced in UUO rats. Immunohistochemical analysis revealed that GSTA3 expression was reduced in renal cortex in UUO rats and patients with obstructive nephropathy. Treating with TGF-β1 down-regulated GSTA3 expression in NRK-52E cells, which have been found to be correlated with the decreased expression in E-cadherin and megalin and increased expression in α-smooth muscle actin. Furthermore, knocking down GSTA3 in NRK-52 cells led to increased production of ROS and tubular EMT, whereas overexpressing GSTA3 ameliorated ROS production and prevented the occurrence of tubular EMT. GSTA3 plays a protective role against tubular EMT in renal fibrosis, suggesting GSTA3 is a potential therapeutic target for RIF.

Indexed as

AnimalsDisease Models, AnimalEpithelial-Mesenchymal TransitionFibronectinsFibrosisGene Expression RegulationGene Knockout TechniquesGlutathione TransferaseHumansKidney CortexKidney DiseasesKidney TubulesMaleRatsReactive Oxygen SpeciesTransforming Growth Factor betaFibronectinsFN1 protein, humanglutathione S-transferase A3-3, humanGlutathione TransferaseReactive Oxygen SpeciesTransforming Growth Factor beta

Identifiers

PMID27602565
PMCPMC5014405
OpenAlexW2517238873

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.