Evidence map›Paper›PMID 40782218›Full record

ArticleJournal of endocrinological investigation2025

Effects of sphingolipid metabolism related genes-SPTLC1, ORMDL3, SPHK1 and S1PR3 polymorphisms on susceptibility to hashimoto's thyroiditis.

Xin Li, Haixia Zhao, Zhifu Xiao

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Article in Journal of endocrinological investigation, 2025. 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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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

  1. Frontiers in genetics · 2026
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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Xin Li *Department of Thyroid Surgery, Shanxi Provincial People's Hospital, 29 Shuangtasi Road, Taiyuan, 030012, Shanxi, China.
Haixia Zhao *Department of Clinical Laboratory, General Hospital of Taiyuan Iron and Steel (Group) Company Limited, Taiyuan, 030003, Shanxi, China.
Zhifu XiaoDepartment of Thyroid Surgery, Shanxi Provincial People's Hospital, 29 Shuangtasi Road, Taiyuan, 030012, Shanxi, China. wangxiaozhifu@126.com.ORCID http://orcid.org/0009-0006-1592-9770

Funding

Youth Project of Shanxi Province Health Commission 2024036
6 · The paper itself

Abstract

backgroundThe destruction of thyroid follicles is an important morphological manifestation of Hashimoto's thyroiditis (HT), and sphingolipid (SPL) metabolism is crucial for maintaining the homeostasis of membrane lipid composition and the stability of the cell membrane. Therefore, the pathogenesis of HT may be related to SPL metabolism. This study aimed to evaluate the associations between SPL metabolism related genes polymorphisms and susceptibility to HT.

methodsSeven SNPs in the SPTLC1, ORMDL3, SPHK1, S1PR1 and S1PR3 were genotyped in 600 HT cases and 600 controls using a MassARRAY platform.

resultsThe mutation alleles of SPTLC1-rs11790991, SPHK1-rs346801 and S1PR3-rs7022797 led to varying degrees of increased HT risk (p < 0.0001), while the ORMDL3-rs8076131 variant was a protective factor for developing HT (p < 0.0001). Carriers of the mutant heterozygous or homozygous genotypes of SPTLC1-rs11790991, SPHK1-rs346801 and S1PR3-rs7022797 exhibited higher risk of HT than those carrying the wild genotypes (p < 0.0001), while the mutant AG/GG genotypes of ORMDL3-rs8076131 resulted in a reduction in HT susceptibility (p < 0.0001). Subgroup analysis showed that the above four potential susceptible SNPs maintained significant in both males and females. However, these significant correlations are manifested under different genetic models.

conclusionsThese results can help identify high-risk populations for HT and suggest that studying SPL metabolism may be a promising direction to explore its pathogenesis.

Indexed as

Genetic Predisposition to DiseaseHashimoto DiseaseMembrane ProteinsSphingosine-1-Phosphate ReceptorsSphingosine KinaseAdultAgedAged, 80 and overCase-Control StudiesFemaleGenotyping TechniquesHumansLipid MetabolismMaleMiddle AgedPolymorphism, Single NucleotideMembrane ProteinsORMDL3 protein, humanS1PR1 protein, humanSerine C-PalmitoyltransferaseSphingolipidssphingosine-1-phosphate receptor-3, humanSphingosine-1-Phosphate ReceptorsSphingosine KinaseSPHK1 protein, humanSPTLC1 protein, humanHashimoto’s thyroiditis (HT)PolymorphismsSphingolipid metabolismSusceptibility

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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.