Evidence map›Paper›PMID 18269193›Full record

ReviewAdvances in experimental medicine and biology2007

Epithelial sodium channels in the adult lung--important modulators of pulmonary health and disease.

Ian C Davis, Sadis Matalon

Open access · greenAbstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Cell fate analysis in fetal mouse lung reveals distinct pathways for TI and TII cell development.American journal of physiology. Lung cellular and molecular physiology · 2019
    Article
  6. Article
  7. Alveolar nonselective channels are ASIC1a/α-ENaC channels and contribute to AFC.American journal of physiology. Lung cellular and molecular physiology · 2017
    Article
  8. Review
  9. Review
  10. Article
  11. Selective targeting of alveolar type II respiratory epithelial cells by anti-surfactant protein-C antibody-conjugated lipoplexes.Journal of controlled release : official journal of the Controlled Release Society · 2015
    Article
  12. Infection of mice with influenza A/WSN/33 (H1N1) virus alters alveolar type II cell phenotype.American journal of physiology. Lung cellular and molecular physiology · 2015
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Structure and function of the mucus clearance system of the lung.Cold Spring Harbor perspectives in medicine · 2013
    Review
  18. Article
  19. Article
  20. ENaCs and ASICs as therapeutic targets.American journal of physiology. Cell physiology · 2012
    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

2 authors at 2 institutions in 1 country.

Ian C DavisDepartment of Veterinary Biosciences, The Ohio State University, Columbus, Ohio, USA.
Sadis Matalon
The Ohio State University · USUniversity of Alabama at Birmingham · US

Funding

PATHOPHYSIOLOGY OF SUBLETHAL OXYGEN IN INJURED LUNGSR01HL031197 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MARK N GILLESPIE, Sadis Matalon · 1985 to 2026
$4.2M
PATHOPHYSIOLOGY OF SUBLETHAL OXYGEN INJURED LUNGSR37HL031197 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MATALON, SADIS · 1997 to 2006
$2.4M
NITRIC OXIDE MEDIATED INJURY TO ALVEOLAR EPITHELIUMR01HL051173 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MATALON, SADIS · 1994 to 2003
$1.5M
Na+ TRANSPORT INHIBITION BY RESPIRATORY SYNCYTIAL VIRUSK01RR017626 · NCRR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DAVIS, IAN CHRISTOPHER · 2003 to 2007
$538k
NCRR NIH HHS RR17626NHLBI NIH HHS HL31197NHLBI NIH HHS HL51173
6 · The paper itself

Abstract

Absorption of excess fluid from the airways and alveolar lumen requires active vectorial transepithelial transport of sodium ions (Na+) by alveolar type II and possibly type I cells. The rate-limiting step in this process is the activity of the heterotrimeric apical membrane epithelial Na+ channel (ENaC). Pharmacologic inhibitors and genetic manipulations that disrupt Na+ transport result in fluid accumulation within the lung and failure of gas exchange. The importance of Na+ transport in the lung is also demonstrated in conditions such as ARDS, where abnormal absorption of Na+ contributes to the pathophysiology of pulmonary disease. ENaC expression and function is influenced by diverse factors, such as oxygen tension, glucocorticoids, and cytoskeletal proteins. In addition, ENaC dysfunction has been shown to be induced by purinergic nucleotide activation of P2Y receptors (in paramyxoviral bronchiolitis) and reactive species (in acute lung injury). Finally, beta-adrenergic agonists have been shown experimentally to reverse defects in ENaC function, and improve hypoxemia and pulmonary edema, and may provide a novel therapeutic modality for ARDS, although some viral lung pathogens appear to induce insensitivity to their actions.

Indexed as

Adrenergic beta-AgonistsAdultEpithelial Sodium ChannelsHumansLungLung DiseasesRisk FactorsSodiumAdrenergic beta-AgonistsEpithelial Sodium ChannelsSodium

Identifiers

PMID18269193
PMCPMC7122934
OpenAlexW68731548

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.