Evidence map›Paper›PMID 41646970›Full record

ArticleFrontiers in immunology2025

Cross-tissue transcriptome-wide association identify novel T1D susceptibility genes and drug candidates.

Yiming Liu, Yu Cao, Yaohui Jiang

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Yiming Liu *Department of Cardiology, National Cardiovascular Disease Regional Center for Anhui, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.
Yu Cao *Department of Endocrinology, The Third Xiangya Hospital of Central South University, Science and Education Building, Changsha, Hunan, China.
Yaohui JiangDepartment of Cardiology, Fuwai Central China Cardiovascular Hospital, Henan Key Laboratory of Coronary Heart Disease Control & Prevention, Central China Fuwai Hospital of Zhengzhou University, Zhengzhou, Henan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The genetic mechanisms underlying type 1 diabetes (T1D) remain incompletely understood, limiting the development of targeted therapies. Methods: We performed an integrative genetic analysis to identify T1D susceptibility genes and therapeutic targets. This included a cross-tissue transcriptome-wide association study (TWAS) to pinpoint genes with genetically predicted expression associated with T1D risk, followed by Mendelian randomization to infer causality. Identified genes were further characterized through pathway, cell-type enrichment, drug prediction, molecular docking, and phenome-wide association studies. Results: We identified ten genes associated with T1D risk, seven of which (ELK4, PHACTR4, MAST2, ST7L, C1orf216, SULT1A2, and WFS1) are novel candidates in this context. Three genes (ELK4, SULT1A2, and WFS1) were prioritized as druggable targets, with COMPOUND 5G and DCLK1-IN-1 emerging as potential therapeutic agents through computational analyses. Conclusion: Our study reveals novel genetic associations and immune-related pathways in T1D pathogenesis, and proposes specific genes and compounds as promising focal points for future mechanistic and therapeutic exploration.

Indexed as

Diabetes Mellitus, Type 1Genetic Predisposition to DiseaseTranscriptomeGene Expression ProfilingGenome-Wide Association StudyHumansMendelian Randomization AnalysisMolecular Docking SimulationPolymorphism, Single Nucleotidecolocalizationcross-tissue TWASMendelian randomizationsingle-cell sequencingtype 1 diabetes

Identifiers

PMID41646970
PMCPMC12867781

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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.