Evidence map›Paper›PMID 40910294›Full record

ArticleEndocrine, metabolic & immune disorders drug targets2026

Unlocking New Treatment Horizons for Celiac Disease: PRKCD Revealed as a Promising Target through Mendelian Randomization

Jie Zhou, Yixin Xu, Haitao Wang, Kun Wang, Chao Chen

Abstract read
In one paragraph

Article in Endocrine, metabolic & immune disorders drug targets, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

1 citing paper in PubMed.

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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

5 authors.

Jie ZhouDepartment of Gastrointestinal Surgery, The Wujin Hospital Affiliated with Jiangsu University, Changzhou, China.ORCID 0000-0002-4096-1442
Yixin XuDepartment of Gastrointestinal Surgery, The Wujin Hospital Affiliated with Jiangsu University, Changzhou, China.
Haitao WangDepartment of Gastrointestinal Surgery, The Third Affiliated Hospital of Soochow University, Changzhou, China.
Kun WangDepartment of Gastrointestinal Surgery, The Wujin Hospital Affiliated with Jiangsu University, Changzhou, China.
Chao ChenDepartment of Gastrointestinal Surgery, The Wujin Hospital Affiliated with Jiangsu University, Changzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCeliac Disease (CeD) is a serious, lifelong autoimmune condition. There remains a significant unmet medical need for effective pharmacological treatments for CeD.

methodsWe utilized summary statistics for 2,888 druggable genes from the eQTLGen Consortium and the FinnGen Consortium for CeD. In our Mendelian Randomization (MR) analysis, we identified genes associated with CeD that had a false discovery rate (FDR) < 0.05 using the Inverse Variance Weighted (IVW) method. To enhance the reliability of the results, we validated them through colocalization analysis and Summary-data-based Mendelian Randomization (SMR) analyses.

resultsThrough our analysis, we identified 18 druggable genes with a causal relationship to CeD under an FDR < 0.05. Subsequent colocalization and SMR analyses highlighted the PRKCD gene as a potential therapeutic target for CeD (IVW method: Odds Ratio 1.319, 95% Confidence Interval 1.182-1.471, P = 6.85E-07, FDR = 0.002). Additionally, these results have passed horizontal pleiotropy tests, heterogeneity analysis, and leave-one-out sensitivity analysis. DISCUSSION: The identification of PRKCD as a therapeutic target represents a significant advancement in addressing the unmet medical need for CeD treatment. However, the hypothesis that PRKCD contributes to CeD pathogenesis by regulating tight junction proteins and altering intestinal barrier function requires further experimental validation in future studies.

conclusionOur study is the first to identify the PRKCD gene as a potential therapeutic target for treating CeD, providing new insights into the treatment of CeD and guiding the development of corresponding therapeutic drugs.

Indexed as

Celiac DiseaseMendelian Randomization AnalysisProtein Kinase C-deltaGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMolecular Targeted TherapyPolymorphism, Single NucleotideProtein Kinase C-deltaclaudinsdruggable genesintestinal barrier.protein kinase Csingle nucleotide polymorphismTight junctions

Identifiers

PMID40910294
PMCPMC13284647

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