Evidence map›Paper›PMID 31289116›Full record

ArticleThe Journal of experimental medicine2019

Sensing of apoptotic cells through Axl causes lung basal cell proliferation in inflammatory diseases.

Naoya Fujino, Oliver J Brand, David J Morgan, Toshifumi Fujimori, Aleksander M Grabiec, Christopher P Jagger, Rose A Maciewicz, Mitsuhiro Yamada, Koji Itakura, Hisatoshi Sugiura and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. The persistent inflammation in COPD: is autoimmunity the core mechanism?European respiratory review : an official journal of the European Respiratory Society · 2024
    Review
  6. Article
  7. Review
  8. Chromosomal instability as an architect of the cancer stemness landscape.Frontiers in cell and developmental biology · 2024
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
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 4 institutions in 4 countries.

Naoya Fujino *Manchester Collaborative Centre for Inflammation Research, the University of Manchester, Manchester, UK nfujino@med.tohoku.ac.jp.
Oliver J Brand *Manchester Collaborative Centre for Inflammation Research, the University of Manchester, Manchester, UK.ORCID 0000-0003-1047-1001
David J Morgan *Manchester Collaborative Centre for Inflammation Research, the University of Manchester, Manchester, UK.ORCID 0000-0002-5085-4093
Toshifumi FujimoriManchester Collaborative Centre for Inflammation Research, the University of Manchester, Manchester, UK.
Aleksander M GrabiecManchester Collaborative Centre for Inflammation Research, the University of Manchester, Manchester, UK.
Christopher P JaggerManchester Collaborative Centre for Inflammation Research, the University of Manchester, Manchester, UK.
Rose A MaciewiczRespiratory, Inflammation, and Autoimmunity Innovative Medicines and Early Development Biotech Unit, AstraZeneca, Gothenburg, Sweden.ORCID 0000-0002-5371-7828
Mitsuhiro YamadaDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
Koji ItakuraDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
Hisatoshi SugiuraDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
Masakazu IchinoseDepartment of Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
Tracy HussellManchester Collaborative Centre for Inflammation Research, the University of Manchester, Manchester, UK tracy.hussell@manchester.ac.uk.ORCID 0000-0001-7186-6141
Tohoku University · JPUniversity of Manchester · GBAstraZeneca (Sweden) · SEJagiellonian University · PL

Funding

Wellcome Trust 202865/Z/16/Z
6 · The paper itself

Abstract

Epithelial cell proliferation, division, and differentiation are critical for barrier repair following inflammation, but the initial trigger for this process is unknown. Here we define that sensing of apoptotic cells by the TAM receptor tyrosine kinase Axl is a critical indicator for tracheal basal cell expansion, cell cycle reentry, and symmetrical cell division. Furthermore, once the pool of tracheal basal cells has expanded, silencing of Axl is required for their differentiation. Genetic depletion of Axl triggers asymmetrical cell division, leading to epithelial differentiation and ciliated cell regeneration. This discovery has implications for conditions associated with epithelial barrier dysfunction, basal cell hyperplasia, and continued turnover of dying cells in patients with chronic inflammatory pulmonary diseases.

Indexed as

ApoptosisAgedAnimalsAxl Receptor Tyrosine KinaseCell CycleCell ProliferationDNAEpitheliumFemaleHomeostasisHumansInflammationLungMaleMice, Inbred C57BLOrthomyxoviridaeAxl Receptor Tyrosine KinaseDNAProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesTrans-ActivatorsTrp63 protein, mouse

Identifiers

PMID31289116
PMCPMC6719415
OpenAlexW2964113213

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.