Evidence map›Paper›PMID 31532390›Full record

ArticleeLife2019

ENaC-mediated sodium influx exacerbates NLRP3-dependent inflammation in cystic fibrosis.

Thomas Scambler, Heledd H Jarosz-Griffiths, Samuel Lara-Reyna, Shelly Pathak, Chi Wong, Jonathan Holbrook, Fabio Martinon, Sinisa Savic, Daniel Peckham, Michael F McDermott

Open access · goldAbstract read
In one paragraph

Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

66 citing papers in PubMed, 103 citations in OpenAlex.

  1. Trial
  2. Molecular mechanisms of NLRP3 inflammasome activation.Experimental & molecular medicine · 2026
    Review
  3. Article
  4. Article
  5. Metallic nanomedicine in cancer immunotherapy.Acta pharmaceutica Sinica. B · 2025
    Review
  6. SECS, drugs, and Rac1&Rho: regulation of EnNaC in vascular endothelial cells.Pflugers Archiv : European journal of physiology · 2025
    Article
  7. ENaC contributes to macrophage dysfunction in cystic fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Journal of fungi (Basel, Switzerland) · 2025
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

6 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

10 authors at 1 institution in 2 countries.

Thomas Scambler *Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, United Kingdom.ORCID 0000-0003-2468-0218
Heledd H Jarosz-Griffiths *Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, United Kingdom.ORCID 0000-0001-5154-4815
Samuel Lara-ReynaLeeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, United Kingdom.ORCID 0000-0002-9986-5279
Shelly PathakLeeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, United Kingdom.
Chi WongLeeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, United Kingdom.ORCID 0000-0003-2108-1615
Jonathan HolbrookLeeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, United Kingdom.
Fabio MartinonLeeds Cystic Fibrosis Trust Strategic Research Centre, University of Leeds, Leeds, United Kingdom.ORCID 0000-0002-6969-822X
Sinisa SavicLeeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, United Kingdom.ORCID 0000-0001-7910-0554
Daniel Peckham *Leeds Institute of Medical Research, University of Leeds, Leeds, United Kingdom.ORCID 0000-0001-7723-1868
Michael F McDermott *Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, Leeds, United Kingdom.ORCID 0000-0002-1015-0745
University of Leeds · GB

Funding

Consejo Nacional de Ciencia y Tecnología CONACyTCystic Fibrosis Trust SRC009University of Leeds 110 University Scholarship
6 · The paper itself

Abstract

Cystic Fibrosis (CF) is a monogenic disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene, resulting in defective CFTR-mediated chloride and bicarbonate transport, with dysregulation of epithelial sodium channels (ENaC). These changes alter fluid and electrolyte homeostasis and result in an exaggerated proinflammatory response driven, in part, by infection. We tested the hypothesis that NLRP3 inflammasome activation and ENaC upregulation drives exaggerated innate-immune responses in this multisystem disease. We identify an enhanced proinflammatory signature, as evidenced by increased levels of IL-18, IL-1β, caspase-1 activity and ASC-speck release in monocytes, epithelia and serum with CF-associated mutations; these differences were reversed by pretreatment with NLRP3 inflammasome inhibitors and notably, inhibition of amiloride-sensitive sodium (Na

Indexed as

Cell LineCystic FibrosisEpithelial Sodium ChannelsHumansImmunity, InnateInflammationNLR Family, Pyrin Domain-Containing 3 ProteinSodiumEpithelial Sodium ChannelsNLR Family, Pyrin Domain-Containing 3 ProteinSodiumautoinflammationcystic fibrosishumanhuman biologyimmunologyinflammasomeinflammationmedicineNLRP3potassium transportsodium transport

Identifiers

PMID31532390
PMCPMC6764826
OpenAlexW2974842032

What OpenQuestion holds

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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.