Evidence map›Paper›PMID 32448163›Full record

ArticleMolecular medicine (Cambridge, Mass.)2020

Pirfenidone alleviates pulmonary fibrosis in vitro and in vivo through regulating Wnt/GSK-3β/β-catenin and TGF-β1/Smad2/3 signaling pathways.

Qun Lv, Jianjun Wang, Changqing Xu, Xuqing Huang, Zhaoyang Ruan, Yifan Dai

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed, 1 pooled it
8.4field-weighted citation impact, top 2% 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

117 citing papers in PubMed, 1 synthesis or guideline pooled it, 183 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
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  13. WNT3a induces external anal sphincter fibrosis and dysfunction in rabbits.American journal of physiology. Gastrointestinal and liver physiology · 2026
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  16. Loading of therapeutic cell penetrating peptides into extracellular vesicles for pulmonary fibrosis.Journal of controlled release : official journal of the Controlled Release Society · 2026
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  17. Article
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  20. Article

57 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Qun LvDepartment of Pneumology, The Affiliated Hospital of Hangzhou Normal University, No. 126, Wenzhou Road, Hangzhou, 31000, Zhejiang, China. lvq_qunlv@163.com.ORCID 0000-0003-0393-3802
Jianjun WangDepartment of Pneumology, The Affiliated Hospital of Hangzhou Normal University, No. 126, Wenzhou Road, Hangzhou, 31000, Zhejiang, China.
Changqing XuDepartment of Pneumology, The Affiliated Hospital of Hangzhou Normal University, No. 126, Wenzhou Road, Hangzhou, 31000, Zhejiang, China.
Xuqing HuangDepartment of Pneumology, The Affiliated Hospital of Hangzhou Normal University, No. 126, Wenzhou Road, Hangzhou, 31000, Zhejiang, China.
Zhaoyang RuanDepartment of Pneumology, The Affiliated Hospital of Hangzhou Normal University, No. 126, Wenzhou Road, Hangzhou, 31000, Zhejiang, China.
Yifan DaiDepartment of Pneumology, The Affiliated Hospital of Hangzhou Normal University, No. 126, Wenzhou Road, Hangzhou, 31000, Zhejiang, China.
Affiliated Hospital of Hangzhou Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPirfenidone (PFD) is effective for pulmonary fibrosis (PF), but its action mechanism has not been fully explained. This study explored the signaling pathways involved in anti-fibrosis role of PFD, thus laying a foundation for clinical application.

methodsPulmonary fibrosis mice models were constructed by bleomycin (BLM), and TGF-β1 was used to treat human fetal lung fibroblasts (HLFs). Then, PFD was added into treated mice and cells alone or in combination with β-catenin vector. The pathological changes, inflammatory factors levels, and Collagen I levels in mice lung tissues were assessed, as well as the activity of HLFs was measured. Levels of indices related to extracellular matrix, epithelial-mesenchymal transition (EMT), Wnt/GSK-3β/β-catenin and TGF-β1/Smad2/3 signaling pathways were determined in tissues or cells.

resultsAfter treatment with BLM, the inflammatory reaction and extracellular matrix deposition in mice lung tissues were serious, which were alleviated by PFD and aggravated by the addition of β-catenin. In HLFs, PFD reduced the activity of HLFs induced by TGF-β1, inhibited levels of vimentin and N-cadherin and promoted levels of E-cadherin, whereas β-catenin produced the opposite effects to PFD. In both tissues and cells, Wnt/GSK-3β/β-catenin and TGF-β1/Smad2/3 signaling pathways were activated, which could be suppressed by PFD.

conclusionsPFD alleviated pulmonary fibrosis in vitro and in vivo through regulating Wnt/GSK-3β/β-catenin and TGF-β1/Smad2/3 signaling pathways, which might further improve the action mechanism of anti-fibrosis effect of PFD.

Indexed as

AnimalsCell SurvivalDisease Models, AnimalGlycogen Synthase Kinase 3 betaHumansLungMaleMicePulmonary FibrosisPyridonesSignal TransductionSmad2 ProteinSmad3 ProteinTransforming Growth Factor beta1Wnt Signaling PathwayGlycogen Synthase Kinase 3 betapirfenidonePyridonesSmad2 ProteinSmad3 ProteinTransforming Growth Factor beta1BleomycinPirfenidonePulmonary fibrosisSignaling pathwayTGF-β1

Identifiers

PMID32448163
PMCPMC7245944
OpenAlexW3026647502

What OpenQuestion holds

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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.