Evidence map›Paper›PMID 22492740›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012

The CFTR and ENaC debate: how important is ENaC in CF lung disease?

James F Collawn, Ahmed Lazrak, Zsuzsa Bebok, Sadis Matalon

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
9.5field-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

50 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Preclinical evaluation of the epithelial sodium channel inhibitor AZD5634 and implications on human translation.American journal of physiology. Lung cellular and molecular physiology · 2022
    Article
  6. Article
  7. Article
  8. Reply to Eisenhut.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  9. Topical administration of ambroxol eye drops augments tear secretion in rabbits.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2021
    Article
  10. SARS-CoV-2 may hijack GPCR signaling pathways to dysregulate lung ion and fluid transport.American journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

James F CollawnDepartment of Cell, Developmental and Integrative Biology, School of Medicine, University of Alabama at Birmingham, 35294-0005, USA. jcollawn@uab.edu
Ahmed Lazrak
Zsuzsa Bebok
Sadis Matalon
University 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
Prevention and Treatment of Chlorine Gas Induced Injury to the Pulmonary SystemU01ES015676 · NIEHS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MATALON, SADIS · 2006 to 2011
$3.3M
Cell Biology of CFTR in Polarized EpitheliaR01DK060065 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI COLLAWN, JAMES F. · 2003 to 2013
$3.1M
CFTR Biogenesis and Function in EpitheliaR01HL076587 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BEBOK, ZSUZSA · 2004 to 2012
$2.6M
NHLBI NIH HHS 5R01HL031197NHLBI NIH HHS HL076587NHLBI NIH HHS R01 HL031197NHLBI NIH HHS R01 HL076587NIDDK NIH HHS DK060065NIDDK NIH HHS R01 DK060065NIEHS NIH HHS 5U01ES015676NIEHS NIH HHS U01 ES015676
6 · The paper itself

Abstract

Cystic fibrosis (CF) is caused by the loss of the cystic fibrosis transmembrane conductance regulator (CFTR) function and results in a respiratory phenotype that is characterized by dehydrated mucus and bacterial infections that affect CF patients throughout their lives. Much of the morbidity and mortality in CF results from a failure to clear bacteria from the lungs. What causes the defect in the bacterial clearance in the CF lung has been the subject of an ongoing debate. Here we discuss the arguments for and against the role of the epithelial sodium channel, ENaC, in the development of CF lung disease.

Indexed as

AnimalsBacteriaBacterial InfectionsCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorDisease Models, AnimalEpithelial Sodium ChannelsHumansIon TransportLungLung DiseasesMiceMice, TransgenicSwineCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorEpithelial Sodium Channels

Identifiers

PMID22492740
PMCPMC3379041
OpenAlexW2090852087

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.