Evidence map›Paper›PMID 37082606›Full record

ArticleBBA advances2022

Extracellular vesicle microRNAs in celiac disease patients under a gluten-free diet, and in lactose intolerant individuals.

Débora S Lemos, Helen C Beckert, Luana C Oliveira, Fernanda C B Berti, Patricia M M Ozawa, Ingrid L M Souza, Silvio M Zanata, Vânia C S Pankievicz, Thalita R Tuleski, Emanuel M Souza and 7 more

Abstract read
In one paragraph

Article in BBA advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Review
  2. Circulating MicroRNAs and Cytokines Associated with Celiac Disease.Middle East journal of digestive diseases · 2024
    Article
  3. Article
  4. Article
  5. 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

17 authors.

Débora S LemosPostgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba 81531-990, Brazil.
Helen C BeckertPostgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba 81531-990, Brazil.
Luana C OliveiraPostgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba 81531-990, Brazil.
Fernanda C B BertiPostgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba 81531-990, Brazil.
Patricia M M OzawaPostgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba 81531-990, Brazil.
Ingrid L M SouzaDepartment of Basic Pathology and Cell Biology, Federal University of Paraná, Curitiba, Brazil.
Silvio M ZanataDepartment of Basic Pathology and Cell Biology, Federal University of Paraná, Curitiba, Brazil.
Vânia C S PankieviczDepartment of Biochemistry and Molecular Biology, Federal University of Paraná, Curitiba, Brazil.
Thalita R TuleskiDepartment of Biochemistry and Molecular Biology, Federal University of Paraná, Curitiba, Brazil.
Emanuel M SouzaDepartment of Biochemistry and Molecular Biology, Federal University of Paraná, Curitiba, Brazil.
Rosiane V SilvaCarlos Chagas Institute - Fiocruz-PR, Curitiba, Brazil.
Pryscilla F WowkCarlos Chagas Institute - Fiocruz-PR, Curitiba, Brazil.
Maria Luiza Petzl-ErlerPostgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba 81531-990, Brazil.
Rodrigo C AlmeidaDepartment of Biomedical Data Sciences, Molecular Epidemiology, Leiden University Medical Center, Leiden, The Netherlands.
Gabriel Adelman CipollaPostgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba 81531-990, Brazil.
Angelica B W BoldtPostgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba 81531-990, Brazil.
Danielle MalheirosPostgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba 81531-990, Brazil.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCeliac disease (CD) is an autoimmune disorder triggered by an abnormal immunological response to gluten ingestion and is associated with deregulated expression of cellular microRNAs (miRNAs) of the gut mucosa. It is frequently misdiagnosed as lactose intolerance (LI) due to symptom resemblance. Microvilli loss may be counteracted by a rigorous gluten-free diet (GFD).

aimsTo identify altered extracellular vesicle miRNAs from plasma among CD patients on GFD (n=34), lactose intolerant individuals on restrictive diet (n=14) and controls (n=23), and to predict biological pathways in which these altered miRNAs may play a part.

methodsFive different small RNA samples of each group were pooled twice and then screened by new-generation sequencing. Four miRNAs were selected to be quantified by RT-qPCR in the entire sample.

resultsThe levels of four miRNAs - miR-99b-3p, miR-197-3p, miR-223-3p, and miR-374b-5p - differed between CD patients and controls (

conclusionsThese miRNAs may have targets that affect cell death, cell communication, adhesion, and inflammation modulation pathways. Hence, altered miRNA levels could be associated with CD-related aspects and gut mucosa recovery.

Indexed as

Celiac diseaseExtracellular vesiclesGluten-free dietLactose intolerancemicroRNAs

Identifiers

PMID37082606
PMCPMC10074944

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.