Evidence map›Paper›PMID 26432872›Full record

ReviewAmerican journal of physiology. Lung cellular and molecular physiology2015

Role of epithelial sodium channels in the regulation of lung fluid homeostasis.

Sadis Matalon, Rafal Bartoszewski, James F Collawn

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 1 pooled it
7.9field-weighted citation impact, top 2% 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

96 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Beyond respiratory depression: acute and delayed pulmonary responses following aerosolized fentanyl exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2026
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. The scaffold protein IQGAP1 regulates the epithelial NaThe Journal of biological chemistry · 2025
    Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Hyperconcentrated mucus in small airways: a mechanistic model for the pathogenesis of paediatric bronchiectasis.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  20. Article

36 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

Sadis MatalonDepartment of Anesthesiology and Perioperative Medicine, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama; Department of Cell, Developmental, and Integrative Biology, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama; Pulmonary Injury and Repair Center, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama; Gregory Fleming James Cystic Fibrosis Center, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama; and.
Rafal BartoszewskiDepartment of Biology and Pharmaceutical Botany, Medical University of Gdansk, Gdansk, Poland.
James F CollawnDepartment of Cell, Developmental, and Integrative Biology, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama; Pulmonary Injury and Repair Center, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama; Gregory Fleming James Cystic Fibrosis Center, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama; and jcollawn@uab.edu.
University of Alabama at Birmingham · USGdańsk Medical University · PL

Funding

Bromine Inhalation Induced Lung Injury: Novel Mechanisms and Treatment StrategiesU01ES026458 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MATALON, SADIS · 2015 to 2019
$3.9M
Cell Biology of CFTR in Polarized EpitheliaR01DK060065 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI COLLAWN, JAMES F. · 2003 to 2013
$3.1M
Central Role of Heme Oxygenase in Reversing Bromine Morbidity and MortalityR21ES025423 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AGARWAL, ANUPAM, MATALON, SADIS · 2014 to 2015
$771k
Mitochondrial Bioenergetic Dysfunction and Chlorine ToxicityR21ES024027 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DARLEY-USMAR, VICTOR M, MATALON, SADIS · 2013 to 2014
$735k
Mechanisms and countermeasures of halogen-induced injury to pregnant miceR21ES026829 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI JILLING, TAMAS SANDOR, MATALON, SADIS · 2015 to 2015
$351k
NHLBI NIH HHS 2R01 HL-0311971NIDDK NIH HHS R01 DK-060065NIEHS NIH HHS 1U01 ES-026458-01A1NIEHS NIH HHS 5R21 ES-024027-02NIEHS NIH HHS R21 ES-025423-01NIEHS NIH HHS R21 ES026829NIEHS NIH HHS U01 ES026458
6 · The paper itself

Abstract

In utero, fetal lung epithelial cells actively secrete Cl(-) ions into the lung air spaces while Na(+) ions follow passively to maintain electroneutrality. This process, driven by an electrochemical gradient generated by the Na(+)-K(+)-ATPase, is responsible for the secretion of fetal fluid that is essential for normal lung development. Shortly before birth, a significant upregulation of amiloride-sensitive epithelial channels (ENaCs) on the apical side of the lung epithelial cells results in upregulation of active Na(+) transport. This process is critical for the reabsorption of fetal lung fluid and the establishment of optimum gas exchange. In the adult lung, active Na(+) reabsorption across distal lung epithelial cells limits the degree of alveolar edema in patients with acute lung injury and cardiogenic edema. Cl(-) ions are transported either paracellularly or transcellularly to preserve electroneutrality. An increase in Cl(-) secretion across the distal lung epithelium has been reported following an acute increase in left atrial pressure and may result in pulmonary edema. In contrast, airway epithelial cells secrete Cl(-) through apical cystic fibrosis transmembrane conductance regulator and Ca(2+)-activated Cl(-) channels and absorb Na(+). Thus the coordinated action of Cl(-) secretion and Na(+) absorption is essential for maintenance of the volume of epithelial lining fluid that, in turn, maximizes mucociliary clearance and facilitates clearance of bacteria and debris from the lungs. Any factor that interferes with Na(+) or Cl(-) transport or dramatically upregulates ENaC activity in airway epithelial cells has been associated with lung diseases such as cystic fibrosis or chronic obstructive lung disease. In this review we focus on the role of the ENaC, the mechanisms involved in ENaC regulation, and how ENaC dysregulation can lead to lung pathology.

Indexed as

HomeostasisBody FluidsCholineEpithelial Sodium ChannelsHumansLungOxidative StressCholineEpithelial Sodium Channelsoxidative stressplasminogen activatorstem cellssteroid hormonesβ-adrenergic agonists

Identifiers

PMID26432872
PMCPMC4669342
OpenAlexW2208098683

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.