Evidence map›Paper›PMID 34428336›Full record

ArticleJournal of cellular and molecular medicine2021

MicroRNA-205-5p targets E2F1 to promote autophagy and inhibit pulmonary fibrosis in silicosis through impairing SKP2-mediated Beclin1 ubiquitination.

Qingzeng Qian, Qinghua Ma, Bin Wang, Qingqiang Qian, Changsong Zhao, Fumin Feng, Xiaona Dong

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Multi-omics reveals a novel Cxcr4Clinical and translational medicine · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. E3 ubiquitin ligase SKP2 limits autophagosome formation duringFrontiers in cellular and infection microbiology · 2026
    Article
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  8. Review
  9. Article
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  11. Article
  12. 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 3 institutions in 1 country.

Qingzeng QianSchool of Public Health, North China University of Science and Technology, Tangshan, China.
Qinghua MaDepartment of Preventive Health, The Third People's Hospital of Xiangcheng District in Suzhou, Suzhou, China.
Bin WangDepartment of Pediatrics, North China University of Science and Technology Affiliated Hospital, Tangshan, China.
Qingqiang QianDepartment of Neurology, Tangshan Gongren Hospital, Tangshan, China.
Changsong ZhaoDepartment of Emergency, Tangshan Hospital of Traditional Chinese Medicine, Tangshan, China.
Fumin FengSchool of Public Health, North China University of Science and Technology, Tangshan, China.
Xiaona DongDepartment of Respiratory Medicine, Tangshan People's Hospital, Tangshan, China.ORCID 0000-0001-8808-7689
North China University of Science and Technology · CNTangshan People's Hospital · CNNorth China University of Science and Technology Affiliated Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Silicosis is an occupational disease characterized by extensive pulmonary fibrosis, and the underlying pathological process remains uncertain. Herein, we explored the molecular mechanism by which microRNA-205-5p (miR-205-5p) affects the autophagy of alveolar macrophages (AMs) and pulmonary fibrosis in mice with silicosis through the E2F transcription factor 1 (E2F1)/S-phase kinase-associated protein 2 (SKP2)/Beclin1 axis. Alveolar macrophages (MH-S cells) were exposed to crystalline silica (CS) to develop an in vitro model, and mice were treated with CS to establish an in vivo model. Decreased Beclin1 and increased SKP2 and E2F1 were identified in mice with silicosis. We silenced or overexpressed miR-205-5p, E2F1, SKP2 and Beclin1 to investigate their potential roles in pulmonary fibrosis in vivo and autophagy in vitro. Recombinant adenovirus mRFP-GFP-LC3 was transduced into the MH-S cells to assay autophagic flow. Knocking down Beclin1 promoted pulmonary fibrosis and suppressed the autophagy. Co-immunoprecipitation and ubiquitination assays suggested that SKP2 induced K48-linked ubiquitination of Beclin1. Furthermore, chromatin immunoprecipitation-PCR revealed the site where E2F1 bound to the SKP2 promoter between 1638 bp and 1645 bp. As shown by dual-luciferase reporter gene assay, the transfection with miR-205-5p mimic inhibited the luciferase activity of the wild-type E2F1 3'untranslated region, suggesting that miR-205-5p targeted E2F1. Additionally, miR-205-5p overexpression increased autophagy and reduced the pulmonary fibrosis, while overexpression of E2F1 or SKP2 or inhibition of Beclin1 could annul this effect. The current study elucidated that miR-205-5p targeted E2F1, thereby inhibiting SKP2-mediated Beclin1 ubiquitination to promote macrophage autophagy and inhibit pulmonary fibrosis in mice with silicosis.

Indexed as

AnimalsAutophagyBeclin-1Cell LineDatabases, GeneticDisease Models, AnimalE2F1 Transcription FactorGene Expression ProfilingGene Expression RegulationHumansImmunohistochemistryMacrophages, AlveolarMiceMicroRNAsModels, BiologicalPromoter Regions, GeneticBeclin-1E2F1 protein, humanE2F1 Transcription FactorMicroRNAsMIR205, humanSKP2 protein, humanS-Phase Kinase-Associated ProteinsBeclin1 ubiquitinationE2F1macrophage autophagyMicroRNA-205-5ppulmonary fibrosissilicosisSKP2

Identifiers

PMID34428336
PMCPMC8500965
OpenAlexW3193532965

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.