Evidence map›Paper›PMID 28634110›Full record

ArticleGastroenterology2017

Restoration of CFTR Activity in Ducts Rescues Acinar Cell Function and Reduces Inflammation in Pancreatic and Salivary Glands of Mice.

Mei Zeng, Mitchell Szymczak, Malini Ahuja, Changyu Zheng, Hongen Yin, William Swaim, John A Chiorini, Robert J Bridges, Shmuel Muallem

Open access · greenAbstract read
In one paragraph

Article in Gastroenterology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 2 pooled it
6.7field-weighted citation impact, top 3% 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, 2 syntheses or guidelines pooled it, 83 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. An open-label extension study of ivacaftor in children with CF and a CFTR gating mutation initiating treatment at age 2-5 years (KLIMB).Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2019
    Trial
  4. Article
  5. Role of Innate Oral Immunity and the Salivary Fluid in Inflammatory Bowel Disease.Cellular and molecular gastroenterology and hepatology · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Exosomes as immunomodulators in autoimmune inflammation: implications for primary Sjögren's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Dysregulated CaeLife · 2024
    Article
  14. Dysregulated CabioRxiv : the preprint server for biology · 2024
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article
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

9 authors at 3 institutions in 2 countries.

Mei ZengMolecular Physiology and Therapeutics Branch, National Institutes of Health, National Institute of Dental and Craniofacial Research, Bethesda, Maryland; North Sichuan Medical College, Sichuan, China.
Mitchell SzymczakMolecular Physiology and Therapeutics Branch, National Institutes of Health, National Institute of Dental and Craniofacial Research, Bethesda, Maryland.
Malini AhujaMolecular Physiology and Therapeutics Branch, National Institutes of Health, National Institute of Dental and Craniofacial Research, Bethesda, Maryland.
Changyu ZhengMolecular Physiology and Therapeutics Branch, National Institutes of Health, National Institute of Dental and Craniofacial Research, Bethesda, Maryland.
Hongen YinMolecular Physiology and Therapeutics Branch, National Institutes of Health, National Institute of Dental and Craniofacial Research, Bethesda, Maryland.
William SwaimMolecular Physiology and Therapeutics Branch, National Institutes of Health, National Institute of Dental and Craniofacial Research, Bethesda, Maryland.
John A ChioriniMolecular Physiology and Therapeutics Branch, National Institutes of Health, National Institute of Dental and Craniofacial Research, Bethesda, Maryland.
Robert J BridgesDepartment of Physiology and Biophysics, Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois.
Shmuel MuallemMolecular Physiology and Therapeutics Branch, National Institutes of Health, National Institute of Dental and Craniofacial Research, Bethesda, Maryland. Electronic address: shmuel.muallem@nih.gov.
National Institute of Dental and Craniofacial Research · USNational Institutes of Health · USRosalind Franklin University of Medicine and Science · US

Funding

Ca2+ signaling and HCO3- secretion by exocrine glandsZIADE000735 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI MUALLEM, SHMUEL · 2010 to 2025
$43.1M
Adeno-associated Virus Biology And Utilization For Gene TransferZIADE000695 · NIDCR · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · PI CHIORINI, JAY · 2009 to 2025
$36.6M
Intramural NIH HHS ZIA DE000735
6 · The paper itself

Abstract

BACKGROUND &

aimsSjögren's syndrome and autoimmune pancreatitis are disorders with decreased function of salivary, lacrimal glands, and the exocrine pancreas. Nonobese diabetic/ShiLTJ mice and mice transduced with the cytokine BMP6 develop Sjögren's syndrome and chronic pancreatitis and MRL/Mp mice are models of autoimmune pancreatitis. Cystic fibrosis transmembrane conductance regulator (CFTR) is a ductal Cl

methodsWe treated the mice models with the CFTR corrector C18 and the potentiator VX770. Glandular, ductal, and acinar cells damage, infiltration, immune cells and function were measured in vivo and in isolated duct/acini.

resultsIn the disease models, CFTR expression is markedly reduced. The salivary glands and pancreas are inflamed with increased fibrosis and tissue damage. Treatment with VX770 and, in particular, C18 restored salivation, rescued CFTR expression and localization, and nearly eliminated the inflammation and tissue damage. Transgenic overexpression of CFTR exclusively in the duct had similar effects. Most notably, the markedly reduced acinar cell Ca

conclusionsOur findings reveal that correcting ductal function is sufficient to rescue acinar cell function and suggests that CFTR correctors are strong candidates for the treatment of Sjögren's syndrome and pancreatitis.

Indexed as

Genetic TherapyAcinar CellsAminophenolsAnimalsAquaporin 5Autoimmune DiseasesBone Morphogenetic Protein 6Calcium SignalingChloride Channel AgonistsCyclopropanesCystic Fibrosis Transmembrane Conductance RegulatorDisease Models, AnimalFemaleInositol 1,4,5-Trisphosphate ReceptorsMice, Inbred MRL lprMice, Inbred NODAminophenolsAqp5 protein, mouseAquaporin 5Bone Morphogenetic Protein 6Chloride Channel AgonistsCyclopropanesCystic Fibrosis Transmembrane Conductance RegulatorInositol 1,4,5-Trisphosphate ReceptorsivacaftorORAI1 ProteinOrai1 protein, mouseQuinolonesCFTRDuctPancreatitisSjögren's syndrome

Identifiers

PMID28634110
PMCPMC5623154
OpenAlexW2765407986

What OpenQuestion holds

Textmetadata
LicenceTDM
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.