Evidence map›Paper›PMID 42706779›Full record

ArticleMediators of inflammation2026

Exploring Causal Links Between 91 Circulating Inflammatory Proteins and Hashimoto's Thyroiditis: A Bidirectional Mendelian Randomization Study.

Shuting Ding, Weiqiang Su, Minghao Wu, Min Fu, Meng Wang, Hongzhi Ji, Bin Yang, Zhen Zhang, Chenyu Ma, Jiani Pan and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Mediators of inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
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

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

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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.

  1. 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

15 authors.

Shuting DingSchool of Public Health, Shandong Second Medical University, Weifang, China.ORCID https://orcid.org/0009-0008-0869-4381
Weiqiang SuSchool of Public Health, Shandong Second Medical University, Weifang, China.ORCID https://orcid.org/0009-0001-6718-3468
Minghao WuSchool of Public Health, Shandong Second Medical University, Weifang, China.ORCID https://orcid.org/0009-0008-2960-5210
Min FuDepartment of Pharmacology, The First Affiliated Hospital of Shandong Second Medical University, Weifang, China.
Meng WangDepartment of Hepatobiliary, The Affiliated Hospital of Shandong Second Medical University, Weifang, China.
Hongzhi JiDepartment of Respiratory, The Affiliated Hospital of Shandong Second Medical University, Weifang, China.
Bin YangDepartment of Imaging, Baoji Maternal and Child Health Hospital, Baoji, China.
Zhen ZhangSchool of Public Health, Shandong Second Medical University, Weifang, China.
Chenyu MaSchool of Public Health, Shandong Second Medical University, Weifang, China.ORCID https://orcid.org/0009-0009-7517-3110
Jiani PanSchool of Public Health, Shandong Second Medical University, Weifang, China.
Xue DiSchool of Public Health, Shandong Second Medical University, Weifang, China.
Xin ZhangSchool of Public Health, Shandong Second Medical University, Weifang, China.ORCID https://orcid.org/0009-0001-2583-4795
Xiaohua ZhaoDepartment of Respiratory, The Affiliated Hospital of Shandong Second Medical University, Weifang, China.ORCID https://orcid.org/0009-0008-0934-7488
Xiaodong SunDepartment of Endocrinology, The Affiliated Hospital of Shandong Second Medical University, Weifang, China.ORCID https://orcid.org/0000-0001-7775-2823
Yujia KongSchool of Public Health, Shandong Second Medical University, Weifang, China.ORCID https://orcid.org/0000-0002-3806-1613

Funding

National Natural Science Foundation of China 82003560National Natural Science Foundation of China 82170865Natural Science Foundation of Shandong Province ZR2020MH340Science and Technology Program of Shaanxi Province 2024SF-YBXM-256
6 · The paper itself

Abstract

backgroundIncreasing evidence has linked inflammation to Hashimoto's thyroiditis (HT) etiology. However, the causal role of circulating inflammatory proteins in HT remains uncertain. To investigate this, we conducted a bidirectional Mendelian randomization (MR) study.

methodsGenetic data for 91 inflammatory proteins and HT were sourced from publicly available GWAS databases. The PhenoScanner database was then searched for pleiotropic SNPs associated with potential confounders. Inverse variance weighted (IVW) analysis was used as the primary analysis, simultaneously supplemented by five sensitivity analyses to strengthen the results.

resultsThe results revealed that, after false discovery rate (FDR) correction, interleukin (IL)-12p40 was causally associated with increased risk of HT (OR [95% CI] = 1.295 [1.172, 1.431], p = 3.66 × 10

conclusionThis study suggests that IL-12p40 is probably one of the factors correlated with HT etiology, contributing to a better understanding of the pathogenesis of HT and underscoring the potential for therapeutic interventions targeting inflammatory proteins.

Indexed as

Hashimoto DiseaseMendelian Randomization AnalysisGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansInflammationInterleukin-12 Subunit p40Polymorphism, Single NucleotideInterleukin-12 Subunit p40causal inferenceHashimoto’s thyroiditisinflammationinflammatory proteinsMendelian randomization

Identifiers

PMID42706779
PMCPMC13550872

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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.