ArticleScientific reports2025
Genetic associations of plasma metabolites with immune cells in hyperthyroidism revealed by Mendelian randomization and GWAS-sc-eQTLs xQTLbiolinks analysis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Genome-wide association study identifies toll-like receptor four protein-mediated metabolic remodelling affecting gout pathogenesis.Journal of global health · 2026Observational
- Endometrial immune dysregulation shapes CD8Frontiers in immunology · 2026Article
- Bidirectional Causal Associations Between Plasma Metabolites and Parkinson's Disease.Molecular neurobiology · 2025Article
- Causal relationships between blood metabolites and glioblastoma risk: a large-scale Mendelian randomization study.Discover oncology · 2025Article
- Genetically predicted interleukin 7 levels and neuroblastoma risk combined with analysis of radiation therapy timing effects.Discover oncology · 2025Article
- Comprehensive Mendelian randomization analysis of inflammatory networks in diabetic nephropathy and pituitary adenoma: unveiling complex causal relationships.Discover oncology · 2025Article
- Developing angiogenesis-related prognostic biomarkers and therapeutic strategies in bladder cancer using deep learning and machine learning.Scientific reports · 2025Article
- Proteome-wide Mendelian randomization reveals causal associations between plasma proteins and autoimmune thyroid disease.Scientific reports · 2025Article
- Therapeutic Target Discovery for Multiple Myeloma: Identifying Druggable Genes via Mendelian Randomization.Biomedicines · 2025Article
- Blood biochemical landscape and new insights into clinical decision-making for polycystic ovary syndrome in Chinese women: a prospective cohort study.Frontiers in endocrinology · 2025Article
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5 authors.
Funding
Abstract
Mendelian randomization (MR) was employed to investigate the causal relationships between immune cell phenotypes, hyperthyroidism (HD), and potential metabolic mediators. In this study, we acquired 731 immune cell phenotypes from genome-wide association studies (GWAS) (n = 18,622), HD data from the research by Handan Melike Dönertaş et al. (3,731 cases, 480,867 controls), and aggregated statistics of 1,400 blood metabolites from UK Biobank (n = 115,078). Bidirectional MR analysis was performed to explore the causal relationships between the immune cell phenotypes and HD, and two-sample and multi-variable MR were conducted to identify the potential plasma metabolites mediating in HD. In addition, sensitivity analyses were used to evaluate robustness, heterogeneity, and horizontal pleiotropy of results. Single-cell transcriptome-based exploration of potential key molecule and mechanism by which plasma metabolites regulated the immune cell differentiation in HD pathogenesis. Co-localization analysis was using single-cell eQTL (sc-eQTL) data with key molecule to probe genetically shared effects. Two-sample MRshowed that CD25 on naive-mature B cell, CD8 + NKT cell, and thymol sulfate level were found to have causal relationships with HD (P < 0.008). The causal relationship between thymol sulfate and HD were further validated in an independent cohort using the inverse-variance weighted (IVW). In addition, CD25 on naive-mature B cells and CD8 + NKT cells were both negatively correlated with thymol sulfate (P < 0.05). The results remained significant after MR-Egger and MR-PRESSO correction for horizontal pleiotropy and heterogeneity (P > 0.05). Multi-variable MR results showed that CD25 on naive-mature B cell and CD8 + NKT cell mediated 8.67% and 10.4% of the associations between thymol sulfate and HD, respectively. Moreover, thymol sulfate mediated the evolution of CD8 + NKT cells in the immune microenvironment, identifying PTPRC, PTK2B, KDM5A and TIGIT as the key participating molecules. Co-localization analysis showed that the key molecules had significant genetic sharing effects with CD8 + NKT cells (PPH4 > 0.75, R
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