Evidence map›Paper›PMID 34357946›Full record

ArticleToxins2021

In Vitro and In Vivo Antifibrotic Effects of Fraxetin on Renal Interstitial Fibrosis via the ERK Signaling Pathway.

Yi-Hsien Hsieh, Tung-Wei Hung, Yong-Syuan Chen, Yi-Ning Huang, Hui-Ling Chiou, Chu-Che Lee, Jen-Pi Tsai

Open access · goldAbstract read
In one paragraph

Article in Toxins, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Fraxetin alleviates BLM-induced idiopathic pulmonary fibrosis by inhibiting NCOA4-mediated epithelial cell ferroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  7. Article
  8. Article
  9. 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

7 authors at 3 institutions in 1 country.

Yi-Hsien HsiehInstitute of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.ORCID 0000-0003-4942-1888
Tung-Wei HungDivision of Nephrology, Department of Medicine, Chung Shan Medical University Hospital, Taichung 40201, Taiwan.
Yong-Syuan ChenInstitute of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.ORCID 0000-0001-5123-4729
Yi-Ning HuangInstitute of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.
Hui-Ling ChiouSchool of Medical Laboratory and Biotechnology, Chung Shan Medical University, Taichung 40201, Taiwan.
Chu-Che LeeDepartment of Medicine Research, Buddhist Dalin Tzu Chi Hospital, Chiayi 62247, Taiwan.
Jen-Pi TsaiSchool of Medicine, Tzu Chi University, Hualien 97010, Taiwan.ORCID 0000-0001-9405-8649
Chung Shan Medical University · TWChung Shan Medical University Hospital · TWTzu Chi University · TW

Funding

Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation DTCRD110-I-27
6 · The paper itself

Abstract

Fraxetin, a natural derivative of coumarin, is known to have anti-inflammatory, anti-oxidant, and hepatoprotective effects in multiple diseases and in liver fibrosis. Whether fraxetin exerts similar effects against renal fibrosis is unknown. In a Unilateral Ureteral Obstruction (UUO) mouse model of renal fibrosis, fraxetin decreased UUO-induced renal dysfunction with a marked reduction in renal interstitial collagen fibers as detected by Masson's Trichrome staining. Fraxetin treatment also inhibited the expression of α-SMA, Collagen I, Collagen IV, fibronectin, N-cadherin, vimentin, phosphorylated-ERK, and increased the expression of E-cadherin in UUO mice, as shown by immunohistochemical staining and western blot analysis. In vitro studies showed that fraxetin and indoxyl sulfate had no cytotoxic effects on MES13 kidney cells, but that fraxetin significantly decreased IS-induced cell motility and decreased protein expression of α-SMA, N-cadherin, vimentin, and Collagen IV via the ERK-mediated signaling pathway. These findings provide insight into the mechanism underlying fraxetin-induced inhibition of fibrogenesis in renal tissue and suggest that fraxetin treatment may be beneficial for slowing CKD progression.

Indexed as

AnimalsAntifibrotic AgentsCadherinsCoumarinsFibronectinsFibrosisKidneyKidney DiseasesMAP Kinase Signaling SystemMiceSignal TransductionTransforming Growth Factor beta1Ureteral ObstructionUrinary TractAntifibrotic AgentsCadherinsCoumarinsFibronectinsfraxetinTransforming Growth Factor beta1chronic kidney diseaseERKfraxetinindoxyl sulfateα-SMA

Identifiers

PMID34357946
PMCPMC8310265
OpenAlexW3178545105

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.