Evidence map›Paper›PMID 33004927›Full record

ArticleScientific reports2020

Exploring celiac disease candidate pathways by global gene expression profiling and gene network cluster analysis.

Babajan Banaganapalli, Haifa Mansour, Arif Mohammed, Arwa Mastoor Alharthi, Nada Mohammed Aljuaid, Khalidah Khalid Nasser, Aftab Ahmad, Omar I Saadah, Jumana Yousuf Al-Aama, Ramu Elango and 1 more

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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

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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

11 authors at 2 institutions in 1 country.

Babajan Banaganapalli *Department of Genetic Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, 21589, Saudi Arabia.
Haifa Mansour *Department of Genetic Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, 21589, Saudi Arabia.
Arif MohammedDepartment of Biology, College of Science, University of Jeddah, Jeddah, Saudi Arabia.
Arwa Mastoor AlharthiPrincess Al-Jawhara Al-Brahim Center of Excellence in Research of Hereditary Disorders, King Abdulaziz University, Jeddah, Saudi Arabia.
Nada Mohammed AljuaidDepartment of Biological Sciences, Faculty of Science, King Abdulaziz University, Jeddah, Saudi Arabia.
Khalidah Khalid NasserPrincess Al-Jawhara Al-Brahim Center of Excellence in Research of Hereditary Disorders, King Abdulaziz University, Jeddah, Saudi Arabia.
Aftab AhmadDepartment of Health Information Technology, Faculty of Applied Studies, King Abdulaziz University, Jeddah, Saudi Arabia.
Omar I SaadahPediatric Gastroenterology Unit, Department of Pediatrics, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Jumana Yousuf Al-AamaDepartment of Genetic Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, 21589, Saudi Arabia.
Ramu ElangoDepartment of Genetic Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, 21589, Saudi Arabia. relango@kau.edu.sa.
Noor Ahmad ShaikDepartment of Genetic Medicine, Faculty of Medicine, King Abdulaziz University, Jeddah, 21589, Saudi Arabia. nshaik@kau.edu.sa.
King Abdulaziz University · SAJeddah University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Celiac disease (CeD) is a gastrointestinal autoimmune disorder, whose specific molecular basis is not yet fully interpreted. Therefore, in this study, we compared the global gene expression profile of duodenum tissues from CeD patients, both at the time of disease diagnosis and after two years of the gluten-free diet. A series of advanced systems biology approaches like differential gene expression, protein-protein interactions, gene network-cluster analysis were deployed to annotate the candidate pathways relevant to CeD pathogenesis. The duodenum tissues from CeD patients revealed the differential expression of 106 up- and 193 down-regulated genes. The pathway enrichment of differentially expressed genes (DEGs) highlights the involvement of biological pathways related to loss of cell division regulation (cell cycle, p53 signalling pathway), immune system processes (NOD-like receptor signalling pathway, Th1, and Th2 cell differentiation, IL-17 signalling pathway) and impaired metabolism and absorption (mineral and vitamin absorptions and drug metabolism) in celiac disease. The molecular dysfunctions of these 3 biological events tend to increase the number of intraepithelial lymphocytes (IELs) and villous atrophy of the duodenal mucosa promoting the development of CeD. For the first time, this study highlights the involvement of aberrant cell division, immune system, absorption, and metabolism pathways in CeD pathophysiology and presents potential novel therapeutic opportunities.

Indexed as

Gene Expression ProfilingCeliac DiseaseGene Expression RegulationGene Regulatory NetworksHumansMetabolic Networks and PathwaysProtein Interaction Maps

Identifiers

PMID33004927
PMCPMC7529771
OpenAlexW3090900504

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.