ArticleFrontiers in medicine2026
Thyroid follicular cell-derived GDF15 attenuates inflammation and lipid dysregulation in Hashimoto's thyroiditis.
Article in Frontiers in medicine, 2026. 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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Abstract
Introduction: Hashimoto's thyroiditis (HT) is a prevalent autoimmune thyroid disorder, typically triggers localized thyroid inflammation and systemic dyslipidemia, and progression to hypothyroidism. While growth differentiation factor 15 (GDF15) is recognized for its role in lipid metabolism and inflammatory diseases, its specific involvement in HT remains elusive. Methods: We conducted plasma metabolomic profiling in HT patients and matched healthy controls to identify altered metabolic pathways. Correlation analysis was performed between serum GDF15 and clinical indicators. In vitro thyroid follicular cell models and NaI-induced in vivo thyroid inflammatory models were applied with GDF15 overexpression, knockdown, recombinant protein and siRNA treatment to explore the functional role of GDF15. Results: Plasma metabolomic profiling in HT patients revealed that differentially expressed metabolites are predominantly enriched in lipid metabolism pathways. GDF15 expression was increased by 1.98-fold in HT serum compared to controls ( Discussion: Given the limitations of the NaI-induced model and the lack of thyroid-specific genetic manipulation, these findings suggest a significant association between GDF15 and HT, though further research is required to establish definitive causality.
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