Evidence map›Paper›PMID 32811866›Full record

ArticleScientific reports2020

ENaC regulation by phospholipids and DGK explained through mathematical modeling.

Daniel V Olivença, Eberhard O Voit, Francisco R Pinto

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 46% 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

4 citing papers in PubMed, 4 citations in OpenAlex.

  1. 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
  2. Hepatic cholesterol biosynthesis and dioxin-induced dysregulation: A multiscale computational approach.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2023
    Article
  3. Review
  4. 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 2 institutions in 2 countries.

Daniel V OlivençaFaculty of Sciences, BioISI - Biosystems and Integrative Sciences Institute, University of Lisboa, 1749-016, Lisbon, Portugal.ORCID http://orcid.org/0000-0001-5474-2657
Eberhard O VoitThe Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, 950 Atlantic Drive, Atlanta, GA, 30332-2000, USA.ORCID http://orcid.org/0000-0003-1378-3043
Francisco R PintoFaculty of Sciences, BioISI - Biosystems and Integrative Sciences Institute, University of Lisboa, 1749-016, Lisbon, Portugal. frpinto@fc.ul.pt.ORCID http://orcid.org/0000-0002-4217-0054
Georgia Institute of Technology · USUniversity of Lisbon · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cystic fibrosis is a condition caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR). It is also thought to increase the activity of epithelial sodium channels (ENaC). The altered function of these ion channels is one of the causes of the thick dehydrated mucus that characterizes the disease and is partially responsible for recurrent pulmonary infections and inflammation events that ultimately destroy the lungs of affected subjects. Phosphoinositides are signaling lipids that regulate numerous cellular processes and membrane proteins, including ENaC. Inhibition of diacylglycerol kinase (DGK), an enzyme of the phosphoinositide pathway, reduces ENaC function. We propose a computational analysis that is based on the combination of two existing mathematical models: one representing the dynamics of phosphoinositides and the other explaining how phosphatidylinositol 4,5-bisphosphate (PI(4,5)P

Indexed as

Computational BiologyCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorDiacylglycerol KinaseEpithelial Sodium ChannelsHumansInositol PhosphatesIon TransportModels, BiologicalPhospholipidsPhosphotransferases (Alcohol Group Acceptor)Signal Transduction1-phosphatidylinositol-4-phosphate 5-kinaseCFTR protein, humanCystic Fibrosis Transmembrane Conductance RegulatorDiacylglycerol KinaseEpithelial Sodium ChannelsInositol PhosphatesPhospholipidsPhosphotransferases (Alcohol Group Acceptor)

Identifiers

PMID32811866
PMCPMC7435262
OpenAlexW3051215073

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.