Evidence map›Paper›PMID 31076989›Full record

ReviewDigestive diseases and sciences2019

Breaking Down Barriers: How Understanding Celiac Disease Pathogenesis Informed the Development of Novel Treatments.

Francesco Valitutti, Alessio Fasano

Open access · greenAbstract readReview
In one paragraph

Review in Digestive diseases and sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
8.0field-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

46 citing papers in PubMed, 77 citations in OpenAlex.

  1. Did diet compliance and remission reduce oxidative stress in celiac patients?Revista da Associacao Medica Brasileira (1992) · 2024
    Trial
  2. Nutrients · 2026
    Article
  3. Review
  4. Article
  5. New therapies in celiac disease.Current opinion in gastroenterology · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Celiac Disease: Risks of Cross-Contamination and Strategies for Gluten Removal in Food Environments.International journal of environmental research and public health · 2024
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
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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

2 authors at 2 institutions in 2 countries.

Francesco ValituttiPediatric Gastroenterology and Liver Unit, Department of "Maternal-and-Child Health" and Urology, Sapienza University of Rome, Rome, Italy.
Alessio FasanoMucosal Immunology and Biology Research Center, Center for Celiac Research and Treatment and Division of Pediatric Gastroenterology and Nutrition, MassGeneral Hospital for Children, 175 Cambridge Street, CPZS - 574, Boston, MA, 02114, USA. afasano@mgh.harvard.edu.
European Biomedical Research Institute of Salerno · ITSapienza University of Rome · IT

Funding

Microbiome-derived Metabolites Linked to Celiac Disease Onset in Infants at RiskR01DK104344 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI FASANO, ALESSIO · 2016 to 2020
$3.4M
NIDDK NIH HHS R01 DK104344
6 · The paper itself

Abstract

For decades, the pathogenesis of a variety of human diseases has been attributed to increased intestinal paracellular permeability even though scientific evidence supporting this hypothesis has been tenuous. Nevertheless, during the past decade, there have been a growing number of publications focused on human genetics, the gut microbiome, and proteomics, suggesting that loss of mucosal barrier function, particularly in the gastrointestinal tract, may substantially affect antigen trafficking, ultimately causing chronic inflammation, including autoimmunity, in genetically predisposed individuals. The gut mucosa works as a semipermeable barrier in that it permits nutrient absorption and also regulates immune surveillance while retaining potentially harmful microbes and environmental antigens within the intestinal lumen. Celiac disease (CD), a systemic, immune-mediated disorder triggered by gluten in genetically susceptible individuals, is associated with altered gut permeability. Pre-clinical and clinical studies have shown that gliadin, a prolamine component of gluten that is implicated in CD pathogenesis, is capable to disassembling intercellular junctional proteins by upregulating the zonulin pathway, which can be inhibited by the zonulin antagonist larazotide acetate. In this review, we will focus on CD as a paradigm of chronic inflammatory diseases in order to outline the contribution of gut paracellular permeability toward disease pathogenesis; moreover, we will summarize current evidence derived from available clinical trials of larazotide acetate in CD.

Indexed as

AnimalsCeliac DiseaseCholera ToxinGastrointestinal AgentsGlutensHaptoglobinsHumansIntercellular JunctionsIntestinal AbsorptionIntestinal MucosaIntestine, SmallOligopeptidesPermeabilityProtein PrecursorsCholera ToxinGastrointestinal AgentsGlutensHaptoglobinslarazotide acetateOligopeptidesProtein PrecursorszonulinAntigen traffickingAutoimmunityGut permeabilityInflammationTight junctionsZonulin

Identifiers

PMID31076989
PMCPMC6586517
OpenAlexW2943880677

What Socratic 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 Socratic graph.