Evidence map›Paper›PMID 32943844›Full record

ArticleDrug design, development and therapy2020

Emodin Retarded Renal Fibrosis Through Regulating HGF and TGFβ-Smad Signaling Pathway.

Fan Yang, Lu Deng, JinPeng Li, MuHu Chen, Ying Liu, YingChun Hu, Wu Zhong

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
4.4field-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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
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  13. Emodin ameliorates renal injury and fibrosisFrontiers in pharmacology · 2023
    Article
  14. Review
  15. Emodin-Mediated Treatment of Acute Kidney Injury.Evidence-based complementary and alternative medicine : eCAM · 2022
    Review
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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 2 institutions in 1 country.

Fan YangDepartment of Emergency Medicine, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, People's Republic of China.
Lu DengDepartment of Thyroid Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, People's Republic of China.
JinPeng LiDepartment of Thyroid and Breast Surgery, Wuhan University Zhongnan Hospital, Wuhan, Hubei 430071, People's Republic of China.
MuHu ChenDepartment of Emergency Medicine, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, People's Republic of China.
Ying LiuDepartment of Emergency Medicine, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, People's Republic of China.
YingChun HuDepartment of Emergency Medicine, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, People's Republic of China.
Wu ZhongDepartment of Emergency Medicine, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, People's Republic of China.
Affiliated Hospital of Southwest Medical University · CNZhongnan Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRenal fibrosis is a frequently occurring type of chronic kidney disease that can cause end-stage renal disease. It has been verified that emodin or HGF can inhibit the development of renal fibrosis. However, the antifibrotic effect of emodin in combination with HGF remains unclear.

methodsCell viability was detected with CCK8. Gene and protein expression in HK2 cells was detected by qRT-PCR and Western blot, respectively. Moreover, a unilateral ureteral obstruction-induced mouse model of renal fibrosis was established for investigating the antifibrotic effect of emodin in combination with HGF in vivo.

resultsHGF notably increased the expression of collagen II in TGFβ-treated HK2 cells. In addition, HGF-induced increase in collagen II expression was further enhanced by emodin. In contrast, fibronectin, αSMA and Smad2 expression in TGFβ-stimulated HK2 cells was significantly inhibited by HGF and further decreased by combination treatment (emodin plus HGF). Moreover, we found that combination treatment exhibited better antifibrotic effects compared with emodin or HGF in vivo.

conclusionThese data demonstrated that emodin plus HGF exhibited better antifibrotic effects compared with emodin or HGF. As such, emodin in combination with HGF may serve as a new possibilty for treatment of renal fibrosis.

Indexed as

AnimalsCells, CulturedDisease Models, AnimalDose-Response Relationship, DrugEmodinFibrosisHepatocyte Growth FactorHumansKidney DiseasesMiceMice, Inbred C57BLSmad ProteinsStructure-Activity RelationshipTransforming Growth Factor beta1Ureteral ObstructionEmodinHepatocyte Growth FactorSmad ProteinsTransforming Growth Factor beta1combinationemodinfibrosisTGFβ

Identifiers

PMID32943844
PMCPMC7478377
OpenAlexW3083181834

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Registered trials

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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.