Evidence map›Paper›PMID 24661119›Full record

ArticleAmerican journal of respiratory cell and molecular biology2014

Reserve autophagic capacity in alveolar epithelia provides a replicative niche for influenza A virus.

David R Hahn, Cheng-Lun Na, Timothy E Weaver

Open access · greenAbstract read
In one paragraph

Article in American journal of respiratory cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. The common ABCA3American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  4. Article
  5. Article
  6. A review of inflammatory mechanism in airway diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Review
  7. Article
  8. Review
  9. Autophagy in Negative-Strand RNA Virus Infection.Frontiers in microbiology · 2018
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Differential regulation of autophagy and mitophagy in pulmonary diseases.American journal of physiology. Lung cellular and molecular physiology · 2016
    Review
  16. Review
  17. 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

3 authors at 1 institution in 2 countries.

David R HahnPerinatal Institute, Section of Neonatology, Perinatal and Pulmonary Biology, Cincinnati Children's Hospital Medical Center and the University of Cincinnati College of Medicine, Cincinnati, Ohio.
Cheng-Lun Na
Timothy E Weaver
Cincinnati Children's Hospital Medical Center · US

Funding

The Role of Autophagy in the Pathogenesis of interstitial Lung DiseaseR01HL103923 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI WEAVER, TIMOTHY EDWARD · 2011 to 2014
$2.0M
NHLBI NIH HHS R01 HL103923NHLBI NIH HHS R01HL103923
6 · The paper itself

Abstract

Autophagy contributes to cellular homeostasis through metabolite recycling and degradation of cytotoxic protein aggregates and damaged organelles. Although recent studies have established that the requirement for basal autophagy is largely tissue specific, the importance of autophagy for alveolar epithelial cell homeostasis remains an important knowledge gap. In the present study we generated two mouse models, with > 90% or > 50% recombination at the Atg5 locus in the distal respiratory epithelium, to assess the effect of dose-dependent decreases in autophagy on alveolar homeostasis. A 90% decrease in autophagy was well tolerated in young adult mice but resulted in alveolar septal thickening and altered lung mechanics in aged animals, consistent with accumulation of damage over time. By comparison, a 50% decrease in autophagy had no effect on alveolar structure or function throughout the murine life span, indicating that basal autophagy in this compartment exceeds that required for homeostasis. A 50% decrease in autophagy in the bronchoalveolar epithelium significantly attenuated influenza A/H3N2 viral replication, leading to improved lung structure and function and reduced morbidity and mortality after infection. The reserve of autophagic capacity in the alveolar epithelium may provide a niche for replication of influenza A virus.

Indexed as

AutophagyAgingAnimalsAutophagy-Related Protein 5Body WeightFemaleGene DeletionHomeostasisInfluenza A virusLungMaleMiceMicrotubule-Associated ProteinsOrthomyxoviridae InfectionsPhenotypePulmonary AlveoliAtg5 protein, mouseAutophagy-Related Protein 5Microtubule-Associated ProteinsAtg5ciliainfluenza Alung injuryviral burden

Identifiers

PMID24661119
PMCPMC4189491
OpenAlexW2078636734

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.