Evidence map›Paper›PMID 23812636›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013

The Fas/FasL pathway impairs the alveolar fluid clearance in mouse lungs.

Raquel Herrero, Mishie Tanino, Lincoln S Smith, Osamu Kajikawa, Venus A Wong, Steve Mongovin, Gustavo Matute-Bello, Thomas R Martin

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Cardiogenic Pulmonary Edema in Emergency Medicine.Advances in respiratory medicine · 2023
    Review
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  3. Review
  4. Review
  5. Article
  6. Article
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  8. Article
  9. Review
  10. Review
  11. A new experimental model of acid- and endotoxin-induced acute lung injury in rats.American journal of physiology. Lung cellular and molecular physiology · 2016
    Article
  12. Article
  13. Novel regulators of endothelial barrier function.American journal of physiology. Lung cellular and molecular physiology · 2014
    Review
  14. Article
  15. 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

8 authors at 2 institutions in 2 countries.

Raquel HerreroMedical Research Service of the Veterans Affairs Puget Sound Health Care Center, Seattle, WA, USA.
Mishie Tanino
Lincoln S Smith
Osamu Kajikawa
Venus A Wong
Steve Mongovin
Gustavo Matute-Bello
Thomas R Martin
VA Puget Sound Health Care System · USUniversity of Washington · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Sakeneh Zraika · 1986 to 2026
$41.4M
The alveolar epithelium in lung injury and repairR01HL083044 · NHLBI · UNIVERSITY OF WASHINGTON · PI MATUTE-BELLO, GUSTAVO · 2006 to 2010
$2.3M
Oxidant Regulation of Proteolysis in Acute Lung InjuryR01HL075381 · NHLBI · UNIVERSITY OF WASHINGTON · PI FU, XIAOYUN · 2004 to 2008
$1.7M
Acute Lung Injury: Link Between Apoptosis and Fibrosis R01HL081764 · NHLBI · UNIVERSITY OF WASHINGTON · PI MATUTE-BELLO, GUSTAVO · 2007 to 2011
$1.6M
NHLBI NIH HHS HL-075381NHLBI NIH HHS HL-081764NHLBI NIH HHS HL-083044NIDDK NIH HHS P30-DK-17047
6 · The paper itself

Abstract

Alveolar epithelial damage is a critical event that leads to protein-rich edema in acute lung injury (ALI), but the mechanisms leading to epithelial damage are not completely understood. Cell death by necrosis and apoptosis occurs in alveolar epithelial cells in the lungs of patients with ALI. Fas activation induces apoptosis of alveolar epithelial cells, but its role in the formation of lung edema is unclear. The main goal of this study was to determine whether activation of the Fas/Fas ligand pathway in the lungs could alter the function of the lung epithelium, and the mechanisms involved. The results show that Fas activation alters the alveolar barrier integrity and impairs the ability of the lung alveolar epithelium to reabsorb fluid from the air spaces. This result was dependent on the presence of a normal Fas receptor and was not affected by inflammation induced by Fas activation. Alteration of the fluid transport properties of the alveolar epithelium was partially restored by β-adrenergic stimulation. Fas activation also caused apoptosis of alveolar endothelial cells, but this effect was less pronounced than the effect on the alveolar epithelium. Thus, activation of the Fas pathway impairs alveolar epithelial function in mouse lungs by mechanisms involving caspase-dependent apoptosis, suggesting that targeting apoptotic pathways could reduce the formation of lung edema in ALI.

Indexed as

Acute Lung InjuryAdenomaAdrenergic beta-AgonistsAnimalsApoptosisBronchoalveolar Lavage FluidCell Membrane PermeabilityCytokinesFas Ligand Proteinfas ReceptorHumansInflammationIsoproterenolLung NeoplasmsMaleMiceAdrenergic beta-AgonistsCytokinesFas Ligand ProteinFas protein, mousefas ReceptorIsoproterenolacute lung injuryalveolar epithelial fluid transportapoptosisedemaendotheliumepitheliumFas ligand

Identifiers

PMID23812636
PMCPMC3763035
OpenAlexW2118270078

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.