Evidence map›Paper›PMID 33135394›Full record

ArticleJournal of cellular and molecular medicine2020

MiR-503 suppresses fibroblast activation and myofibroblast differentiation by targeting VEGFA and FGFR1 in silica-induced pulmonary fibrosis.

Qiuyun Wu, Lei Han, Wenwen Gui, Feng Wang, Weiwen Yan, Hua Jiang

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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 12% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  5. Mechanisms and Therapeutic Potential of Myofibroblast Transformation in Pulmonary Fibrosis.Journal of respiratory biology and translational medicine · 2025
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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 3 institutions in 1 country.

Qiuyun WuSchool of Public Health, Xuzhou Medical University, Xuzhou, China.ORCID 0000-0003-0669-7120
Lei HanInstitute of Occupational Disease Prevention, Jiangsu Provincial Center for Disease Control and Prevention, Nanjing, China.
Wenwen GuiSchool of Public Health, Xuzhou Medical University, Xuzhou, China.
Feng WangTianjin Institute of Environmental and Operational Medicine, Tianjin, China.
Weiwen YanDepartment of Occupational Medicine and Environmental Health, Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, China.
Hua JiangSchool of Public Health, Xuzhou Medical University, Xuzhou, China.
Xuzhou Medical College · CNJiangsu Provincial Center for Disease Control and Prevention · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inhalation and deposition of crystalline silica particles in the lung can cause pulmonary fibrosis, then leading to silicosis. Given the paucity of effective drugs for silicosis, new insights for understanding the mechanisms of silicosis, including lung fibroblast activation and myofibroblast differentiation, are essential to explore therapeutic strategies. Our previous research showed that the up-regulation of miR-503 alleviated silica-induced pulmonary fibrosis in mice. In this study, we investigated whether miR-503 can regulate the TGF-β1-induced effects in lung fibroblasts. Mimic-based strategies aiming at up-regulating miR-503 were used to discuss the function of miR-503 in vivo and in vitro. We found that the expression level of miR-503 was decreased in fibroblasts stimulated by TGF-β1, and the up-regulation of miR-503 reduced the release of fibrotic factors and inhibited the migration and invasion abilities of fibroblasts. Combined with the up-regulation of miR-503 in a mouse model of silica-induced pulmonary fibrosis, we revealed that miR-503 mitigated the TGF-β1-induced effects in fibroblasts by regulating VEGFA and FGFR1 and then affecting the MAPK/ERK signalling pathway. In conclusion, miR-503 exerted protective roles in silica-induced pulmonary fibrosis and may represent a novel and potent candidate for therapeutic strategies in silicosis.

Indexed as

AnimalsCell DifferentiationCell LineFibroblastsGene Expression RegulationHumansMiceModels, BiologicalMyofibroblastsPulmonary FibrosisRNA InterferenceVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth Factor Avascular endothelial growth factor A, mouseVascular Endothelial Growth Factor Receptor-1miR-503myofibroblast differentiationpulmonary fibrosissilicosis

Identifiers

PMID33135394
PMCPMC7754009
OpenAlexW3097235876

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.