Evidence map›Paper›PMID 31162135›Full record

ArticleThe Journal of clinical investigation2019

Autophagy is required for lung development and morphogenesis.

Behzad Yeganeh, Joyce Lee, Leonardo Ermini, Irene Lok, Cameron Ackerley, Martin Post

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

40 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
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  5. Explant Culture for Studying Lung Development.Methods in molecular biology (Clifton, N.J.) · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Behzad YeganehProgram in Translational Medicine, Peter Gilgan Centre for Research and Learning, Hospital for Sick Children.
Joyce LeeProgram in Translational Medicine, Peter Gilgan Centre for Research and Learning, Hospital for Sick Children.
Leonardo ErminiProgram in Translational Medicine, Peter Gilgan Centre for Research and Learning, Hospital for Sick Children.
Irene LokProgram in Translational Medicine, Peter Gilgan Centre for Research and Learning, Hospital for Sick Children.
Cameron AckerleyProgram in Translational Medicine, Peter Gilgan Centre for Research and Learning, Hospital for Sick Children.
Martin PostProgram in Translational Medicine, Peter Gilgan Centre for Research and Learning, Hospital for Sick Children.
Hospital for Sick Children · CAUniversity of Toronto · CA

Funding

CIHR FDN-143309
6 · The paper itself

Abstract

Bronchopulmonary dysplasia (BPD) remains a major respiratory illness in extremely premature infants. The biological mechanisms leading to BPD are not fully understood, although an arrest in lung development has been implicated. The current study aimed to investigate the occurrence of autophagy in the developing mouse lung and its regulatory role in airway branching and terminal sacculi formation. We found 2 windows of epithelial autophagy activation in the developing mouse lung, both resulting from AMPK activation. Inhibition of AMPK-mediated autophagy led to reduced lung branching in vitro. Conditional deletion of beclin 1 (Becn1) in mouse lung epithelial cells (Becn1Epi-KO), either at early (E10.5) or late (E16.5) gestation, resulted in lethal respiratory distress at birth or shortly after. E10.5 Becn1Epi-KO lungs displayed reduced airway branching and sacculi formation accompanied by impaired vascularization, excessive epithelial cell death, reduced mesenchymal thinning of the interstitial walls, and delayed epithelial maturation. E16.5 Becn1Epi-KO lungs had reduced terminal air sac formation and vascularization and delayed distal epithelial differentiation, a pathology similar to that seen in infants with BPD. Taken together, our findings demonstrate that intrinsic autophagy is an important regulator of lung development and morphogenesis and may contribute to the BPD phenotype when impaired.

Indexed as

Autophagic Cell DeathOrganogenesisAnimalsBeclin-1Bronchopulmonary DysplasiaLungMiceMice, KnockoutBeclin-1Becn1 protein, mouseAutophagyDevelopmentOrganogenesisPulmonary surfactantsPulmonology

Identifiers

PMID31162135
PMCPMC6597208
OpenAlexW2948057470

What OpenQuestion holds

Textmetadata
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.