Evidence map›Paper›PMID 29997053›Full record

ArticleEBioMedicine2018

TGF-β3 Promotes MUC5AC Hyper-Expression by Modulating Autophagy Pathway in Airway Epithelium.

Yun Zhang, Hongmei Tang, Xiefang Yuan, Qin Ran, Xiaoyun Wang, Qi Song, Lei Zhang, Yuhuan Qiu, Xing Wang

Abstract read
In one paragraph

Article in EBioMedicine, 2018. 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
–field-weighted citation impact
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.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. TGF-β: The missing link in obesity-associated airway diseases?Current research in pharmacology and drug discovery · 2021
    Review
  12. Article
  13. Article
  14. Autophagy in chronic lung disease.Progress in molecular biology and translational science · 2020
    Review
  15. TGF-Mediators of inflammation · 2019
    Article
  16. Fibroblast-to-myofibroblast transition in bronchial asthma.Cellular and molecular life sciences : CMLS · 2018
    Review
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

9 authors.

Yun ZhangInflammation & Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, China; First Department of Respiratory Disease, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China; State Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.
Hongmei TangInflammation & Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, China.
Xiefang YuanInflammation & Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, China.
Qin RanFirst Department of Respiratory Disease, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Xiaoyun WangInflammation & Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, China.
Qi SongState Key Laboratory of Quality Research in Chinese Medicine, Macau University of Science and Technology, Macau, China.
Lei ZhangFirst Department of Respiratory Disease, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Yuhuan QiuFirst Department of Respiratory Disease, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
Xing WangInflammation & Allergic Diseases Research Unit, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan 646000, China. Electronic address: wx_eliot_881014@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mucus secretion accumulation in the airways may act as a contributing factor for the development of airflow limitation in severe fetal asthma patients. Accumulated evidences showed that transforming growth factor beta (TGF-β) plays a regulatory role in airway remodeling including mucus hyper-secretion in asthma. However, the detailed molecular mechanisms of TGF-β3 induced MUC5AC hyper-expression in airway epithelium remains unclear. Here, we demonstrated the pivotal roles of autophagy in regulation of MUC5AC hyper-production induced by TGF-β3 in airway epithelium. Our experimental data showed that inhibiting autophagy pathway in repeated ovalbumin (OVA) exposed mice exhibited decreased airway hyper-response and airway inflammation, diminishing the expression of Muc5ac and TGF-β3. Furthermore, our studies demonstrated that autophagy was induced upon exposure to TGF-β3 and then mediated MUC5AC hyper-expression by activating the activator protein-1 (AP-1) in human bronchial epithelial cells. Finally, Smad2/3 pathway was involved in TGF-β3-induced MUC5AC hyper-expressions by promoting autophagy. These data indicated that autophagy was required for TGF-β3 induced airway mucous hyper-production, and that inhibition of autophagy exerted therapeutic benefits for TGF-β3 induced airway mucus secretion.

Indexed as

Up-RegulationAnimalsAsthmaAutophagyBronchiDisease Models, AnimalEpithelial CellsFemaleHumansMiceMucin 5ACOvalbuminSignal TransductionTranscription Factor AP-1Transforming Growth Factor beta3MUC5AC protein, humanMucin 5ACOvalbuminTgfb3 protein, mouseTranscription Factor AP-1Transforming Growth Factor beta3AutophagyMUC5ACSmad2/3TGF-β3

Identifiers

PMID29997053
PMCPMC6085582

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Registered trials

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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.