Evidence map›Paper›PMID 32344567›Full record

ArticlePharmaceutics2020

Senescence of IPF Lung Fibroblasts Disrupt Alveolar Epithelial Cell Proliferation and Promote Migration in Wound Healing.

Kaj E C Blokland, David W Waters, Michael Schuliga, Jane Read, Simon D Pouwels, Christopher L Grainge, Jade Jaffar, Glen Westall, Steven E Mutsaers, Cecilia M Prêle and 2 more

Open access · goldAbstract read
In one paragraph

Article in Pharmaceutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 55 citations in OpenAlex.

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  14. SIRT3/6/7: promising therapeutic targets for pulmonary fibrosis.Frontiers in cell and developmental biology · 2025
    Review
  15. Article
  16. ModulatingAging · 2024
    Article
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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

12 authors at 6 institutions in 3 countries.

Kaj E C BloklandSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, NSW 2308, Australia.ORCID 0000-0002-1807-6359
David W WatersSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, NSW 2308, Australia.
Michael SchuligaSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, NSW 2308, Australia.ORCID 0000-0001-6742-5028
Jane ReadSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, NSW 2308, Australia.
Simon D PouwelsUniversity of Groningen, University Medical Center Groningen, Groningen Research Institute for Asthma and COPD, 9713 GZ Groningen, The Netherlands.
Christopher L GraingeNational Health and Medical Research Council Centre of Research Excellence in Pulmonary Fibrosis, Camperdown, NSW 2050, Australia.
Jade JaffarAllergy, Immunology and Respiratory Medicine, Alfred Hospital, Prahran, Vic 3004, Australia.
Glen WestallAllergy, Immunology and Respiratory Medicine, Alfred Hospital, Prahran, Vic 3004, Australia.
Steven E MutsaersCentre for Cell Therapy and Regenerative Medicine, School of Biomedical Sciences University of Western Australia, Crawley, WA 6009, Australia.
Cecilia M PrêleCentre for Cell Therapy and Regenerative Medicine, School of Biomedical Sciences University of Western Australia, Crawley, WA 6009, Australia.
Janette K BurgessUniversity of Groningen, University Medical Center Groningen, Department of Pathology and Medical Biology, 9713 GZ Groningen, The Netherlands.ORCID 0000-0001-9868-9966
Darryl A KnightSchool of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, NSW 2308, Australia.
University Medical Center Groningen · NLNational Health and Medical Research Council · AUThe Alfred Hospital · AUThe University of Western Australia · AUUniversity of Newcastle Australia · AUProvidence Health Care Research Institute · CA

Funding

CSRD VA 1National Health and Medical Research Council 1099569
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease marked by excessive accumulation of lung fibroblasts (LFs) and collagen in the lung parenchyma. The mechanisms that underlie IPF pathophysiology are thought to reflect repeated alveolar epithelial injury leading to an aberrant wound repair response. Recent work has shown that IPF-LFs display increased characteristics of senescence including growth arrest and a senescence-associated secretory phenotype (SASP) suggesting that senescent LFs contribute to dysfunctional wound repair process. Here, we investigated the influence of senescent LFs on alveolar epithelial cell repair responses in a co-culture system. Alveolar epithelial cell proliferation was attenuated when in co-culture with cells or conditioned media from, senescence-induced control LFs or IPF-LFs. Cell-cycle analyses showed that a larger number of epithelial cells were arrested in G2/M phase when co-cultured with IPF-LFs, than in monoculture. Paradoxically, the presence of LFs resulted in increased A549 migration after mechanical injury. Our data suggest that senescent LFs may contribute to aberrant re-epithelialization by inhibiting proliferation in IPF.

Indexed as

aberrant repairalveolar epithelial cellcell-cycle inhibitionfibroblastsfibrosissenescence

Identifiers

PMID32344567
PMCPMC7238173
OpenAlexW3018118152

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.