Evidence map›Paper›PMID 30636861›Full record

ArticleMolecular vision2018

Nintedanib inhibits TGF-β-induced myofibroblast transdifferentiation in human Tenon's fibroblasts.

Xianchai Lin, Jiamin Wen, Rongjiao Liu, Wuyou Gao, Bo Qu, Minbin Yu

Open access · greenAbstract read
In one paragraph

Article in Molecular vision, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.6field-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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

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  18. Involvement of METTL3/mJournal of molecular histology · 2021
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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

6 authors at 1 institution in 1 country.

Xianchai LinState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Jiamin WenState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Rongjiao LiuState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Wuyou GaoState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Bo QuState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Minbin YuState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: This study aimed to investigate the effect of nintedanib on the conversion of human Tenon's fibroblasts (HTFs) into myofibroblasts and reveal the molecular mechanisms involved. Methods: Primary cultured HTFs were incubated with transforming growth factor β1 (TGF-β1) alone or combined with nintedanib, and cell proliferation and migration were measured by cell counting kit-8 (CCK8) and the scratch wound assay, respectively. HTF contractility was evaluated with a 3D collagen contraction assay. The mRNA and protein levels of α smooth muscle actin (α-SMA) and Snail and the phosphorylation levels of Smad2/3, p38 mitogen-activated protein kinase (p38MAPK), and extracellular signal-regulated kinase ½ (ERK1/2) were determined by quantitative reverse transcription polymerase chain reaction (RT-PCR), western blot, and immunofluorescence staining. Results: Nintedanib inhibited the proliferation and migration of HTFs in a dose-dependent manner. Furthermore, nintedanib prevented HTF myofibroblast differentiation via downregulation of mRNA and protein expression of α-SMA and Snail. A three-dimensional (3D) collagen gel contraction assay demonstrated that nintedanib effectively inhibits myofibroblast contraction induced by TGF-β1. Mechanistically, we revealed that nintedanib reduces the TGF-β1-induced phosphorylation of Smad2/3, p38MAPK, and ERK1/2, suggesting that nintedanib acts through both classic and nonclassic signaling pathways of TGF-β1 to prevent HTF activation. Conclusions: Our study provides new evidence that nintedanib has potent antifibrotic effects in HTFs and suggests that it may be used as a potential therapeutic agent for subconjunctival fibrosis.

Indexed as

ActinsCell MovementCell ProliferationCell TransdifferentiationDose-Response Relationship, DrugFibroblastsGene Expression RegulationHumansIndolesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Myofibroblastsp38 Mitogen-Activated Protein KinasesPhosphorylationPrimary Cell CultureSignal TransductionACTA2 protein, humanActinsIndolesMAPK1 protein, humanMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3nintedanibp38 Mitogen-Activated Protein KinasesSmad2 ProteinSMAD2 protein, humanSmad3 ProteinSMAD3 protein, humanSNAI1 protein, humanSnail Family Transcription FactorsTGFB1 protein, humanTransforming Growth Factor beta1

Identifiers

PMID30636861
PMCPMC6300612
OpenAlexW2971587458

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.