ArticleThe Journal of endocrinology2020
Decreased SIRT1 expression in the peripheral blood of patients with Graves' disease.
Article in The Journal of endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Examining Sirtuin-1 Levels and Inflammation Markers in Behcet's Disease: A Pilot Study.Archives of rheumatology · 2025Article
- Sirtuin family in autoimmune diseases.Frontiers in immunology · 2023Review
- LncRNA RUNX1-IT1 affects the differentiation of Th1 cells by regulating NrCAM transcription in Graves' disease.Cell cycle (Georgetown, Tex.) · 2022Article
- Comprehensive Analysis of lncRNA Expression Profile and the Potential Role of ENST00000604491 in Graves' Disease.Journal of immunology research · 2022Article
- A Global Regulatory Network for Dysregulated Gene Expression and Abnormal Metabolic Signaling in Immune Cells in the Microenvironment of Graves' Disease and Hashimoto's Thyroiditis.Frontiers in immunology · 2022Article
- Analysis of Expression of Different Histone Deacetylases in Autoimmune Thyroid Disease.The Journal of clinical endocrinology and metabolism · 2021Article
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SIRT1, a class III histone/protein deacetylase (HDAC), has been associated with autoimmune diseases. There is a paucity of data about the role of SIRT1 in Graves' disease. The aim of this study was to investigate the role of SIRT1 in the pathogenesis of GD. Here, we showed that SIRT1 expression and activity were significantly decreased in GD patients compared with healthy controls. The NF-κB pathway was activated in the peripheral blood of GD patients. The reduced SIRT1 levels correlated strongly with clinical parameters. In euthyroid patients, SIRT1 expression was markedly upregulated and NF-κB downstream target gene expression was significantly reduced. SIRT1 inhibited the NF-κB pathway activity by deacetylating P65. These results demonstrate that reduced SIRT1 expression and activity contribute to the activation of the NF-κB pathway and may be involved in the pathogenesis of GD.
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Registered trials
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