Evidence map›Paper›PMID 31391462›Full record

ArticleCell death & disease2019

Autophagy inhibition-mediated epithelial-mesenchymal transition augments local myofibroblast differentiation in pulmonary fibrosis.

Charlotte Hill, Juanjuan Li, Dian Liu, Franco Conforti, Christopher J Brereton, Liudi Yao, Yilu Zhou, Aiman Alzetani, Serena J Chee, Ben G Marshall and 10 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
18.1field-weighted citation impact, top 1% 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

110 citing papers in PubMed, 173 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Targeting the senescence‒autophagy axis via p16Signal transduction and targeted therapy · 2026
    Article
  5. Article
  6. Review
  7. Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. A Functional VariantAmerican journal of respiratory cell and molecular biology · 2025
    Article
  19. Review
  20. Review

50 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

20 authors at 7 institutions in 3 countries.

Charlotte HillBiological Sciences, Faculty of Environmental and Life Sciences, University of Southampton, Southampton, SO17 1BJ, UK.
Juanjuan LiBiological Sciences, Faculty of Environmental and Life Sciences, University of Southampton, Southampton, SO17 1BJ, UK.
Dian LiuDepartment of Oncology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Franco ConfortiClinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, SO16 6YD, UK.
Christopher J BreretonClinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, SO16 6YD, UK.
Liudi YaoBiological Sciences, Faculty of Environmental and Life Sciences, University of Southampton, Southampton, SO17 1BJ, UK.
Yilu ZhouBiological Sciences, Faculty of Environmental and Life Sciences, University of Southampton, Southampton, SO17 1BJ, UK.
Aiman AlzetaniNIHR Southampton Biomedical Research Centre, University Hospital Southampton, Southampton, SO16 6YD, UK.
Serena J CheeUniversity Hospital Southampton, Southampton, SO16 6YD, UK.
Ben G MarshallNIHR Southampton Biomedical Research Centre, University Hospital Southampton, Southampton, SO16 6YD, UK.ORCID http://orcid.org/0000-0003-0946-0399
Sophie V FletcherNIHR Southampton Biomedical Research Centre, University Hospital Southampton, Southampton, SO16 6YD, UK.
David HancockOncogene Biology, The Francis Crick Institute, London, NW1 1AT, UK.
Christian H OttensmeierNIHR Southampton Biomedical Research Centre, University Hospital Southampton, Southampton, SO16 6YD, UK.ORCID http://orcid.org/0000-0003-3619-1657
Andrew J SteeleCancer Sciences Unit, University of Southampton, Somers Building, Southampton General Hospital, Southampton, SO16 6YD, UK.ORCID http://orcid.org/0000-0003-0667-1596
Julian DownwardOncogene Biology, The Francis Crick Institute, London, NW1 1AT, UK.ORCID http://orcid.org/0000-0002-2331-4729
Luca RicheldiClinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, SO16 6YD, UK.
Xin LuLudwig Institute for Cancer Research, Nuffield Department of Clinical Medicine, University of Oxford, Oxford, OX3 7DQ, UK.
Donna E DaviesClinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, SO16 6YD, UK.
Mark G JonesClinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, SO16 6YD, UK.ORCID http://orcid.org/0000-0001-6308-6014
Yihua WangBiological Sciences, Faculty of Environmental and Life Sciences, University of Southampton, Southampton, SO17 1BJ, UK. yihua.wang@soton.ac.uk.ORCID http://orcid.org/0000-0001-5561-0648
University Hospital Southampton NHS Foundation Trust · GBUniversity of Southampton · GBSouthampton General Hospital · GBThe Francis Crick Institute · GBTongji Hospital · CNUniversità Cattolica del Sacro Cuore · ITUniversity of Oxford · GB

Funding

Cancer Research UK FC001070Department of HealthMedical Research Council FC001070MRF_ MRF-091-0003-RG-CONFOWellcome Trust 100638/Z/12/ZWellcome Trust FC001070
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF), the prototypic progressive fibrotic interstitial lung disease, is thought to be a consequence of repetitive micro-injuries to an ageing, susceptible alveolar epithelium. Ageing is a risk factor for IPF and incidence has been demonstrated to increase with age. Decreased (macro)autophagy with age has been reported extensively in a variety of systems and diseases, including IPF. However, it is undetermined whether the role of faulty autophagy is causal or coincidental in the context of IPF. Here, we report that in alveolar epithelial cells inhibition of autophagy promotes epithelial-mesenchymal transition (EMT), a process implicated in embryonic development, wound healing, cancer metastasis and fibrosis. We further demonstrate that this is attained, at least in part, by increased p62/SQSTM1 expression that promotes p65/RELA mediated-transactivation of an EMT transcription factor, Snail2 (SNAI2), which not only controls EMT but also regulates the production of locally acting profibrogenic mediators. Our data suggest that reduced autophagy induces EMT of alveolar epithelial cells and can contribute to fibrosis via aberrant epithelial-fibroblast crosstalk.

Indexed as

A549 CellsAgingAlveolar Epithelial CellsAutophagyCell DifferentiationEpithelial-Mesenchymal TransitionFibroblastsHumansIdiopathic Pulmonary FibrosisLungLung NeoplasmsMyofibroblastsPrimary Cell CultureRisk FactorsSequestosome-1 ProteinSnail Family Transcription FactorsRELA protein, humanSequestosome-1 ProteinSNAI2 protein, humanSnail Family Transcription FactorsSQSTM1 protein, humanTranscription Factor RelATranscription Factors

Identifiers

PMID31391462
PMCPMC6685977
OpenAlexW2963688247

What OpenQuestion holds

Textmetadata
LicenceTDM
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.