Evidence map›Paper›PMID 33058500›Full record

ArticleJournal of cellular and molecular medicine2020

Polydatin inhibits ZEB1-invoked epithelial-mesenchymal transition in fructose-induced liver fibrosis.

Xiaojuan Zhao, Yanzi Yang, Hanwen Yu, Wenyuan Wu, Yang Sun, Ying Pan, Lingdong Kong

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

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  8. Reviewing the Regulators of COL1A1.International journal of molecular sciences · 2023
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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

7 authors at 1 institution in 1 country.

Xiaojuan ZhaoState Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, China.ORCID 0000-0003-3973-5875
Yanzi YangState Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, China.
Hanwen YuState Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, China.
Wenyuan WuState Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, China.
Yang SunState Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, China.
Ying PanState Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, China.
Lingdong KongState Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, China.
Nanjing University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High fructose intake is a risk factor for liver fibrosis. Polydatin is a main constituent of the rhizome of Polygonum cuspidatum, which has been used in traditional Chinese medicine to treat liver fibrosis. However, the underlying mechanisms of fructose-driven liver fibrosis as well as the actions of polydatin are not fully understood. In this study, fructose was found to promote zinc finger E-box binding homeobox 1 (ZEB1) nuclear translocation, decrease microRNA-203 (miR-203) expression, increase survivin, activate transforming growth factor β1 (TGF-β1)/Smad signalling, down-regulate E-cadherin, and up-regulate fibroblast specific protein 1 (FSP1), vimentin, N-cadherin and collagen I (COL1A1) in rat livers and BRL-3A cells, in parallel with fructose-induced liver fibrosis. Furthermore, ZEB1 nuclear translocation-mediated miR-203 low-expression was found to target survivin to activate TGF-β1/Smad signalling, causing the EMT in fructose-exposed BRL-3A cells. Polydatin antagonized ZEB1 nuclear translocation to up-regulate miR-203, subsequently blocked survivin-activated TGF-β1/Smad signalling, which were consistent with its protection against fructose-induced EMT and liver fibrosis. These results suggest that ZEB1 nuclear translocation may play an essential role in fructose-induced EMT in liver fibrosis by targeting survivin to activate TGF-β1/Smad signalling. The suppression of ZEB1 nuclear translocation by polydatin may be a novel strategy for attenuating the EMT in liver fibrosis associated with high fructose diet.

Indexed as

Epithelial-Mesenchymal TransitionActive Transport, Cell NucleusAnimalsCadherinsCollagen Type ICollagen Type I, alpha 1 ChainFructoseGlucosidesLiver CirrhosisMaleMicroRNAsRatsRats, Sprague-DawleySignal TransductionStilbenesTransforming Growth Factor beta1CadherinsCollagen Type ICollagen Type I, alpha 1 ChainFructoseGlucosidesMicroRNAsMIRN203 microRNA, ratpolydatinStilbenesTgfb1 protein, ratTransforming Growth Factor beta1ZEB1 protein, ratZinc Finger E-box-Binding Homeobox 1EMTexcess fructose intakemiR-203polydatinZEB1

Identifiers

PMID33058500
PMCPMC7701525
OpenAlexW3092998307

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.