Abstract
Objective Hashimoto's thyroiditis, also known as chronic lymphocytic thyroiditis, is a common autoimmune thyroiditis, which mostly occurs in young and middle-aged women. It can be manifested as hyperthyroidism in the early stage; hypothyroidism may appear with the progression of the disease. Studies have shown that multiple factors such as heredity, environment, and autoimmunity are involved in the pathogenesis, but the specific mechanism is not clear. In our study, we tried to find key genes and potential molecular mechanisms of Hashimoto's thyroiditis to provide new ideas for the therapeutic targets of Hashimoto's thyroiditis. Method GSE138198 and GSE54958 were downloaded from the GEO database, and two datasets were combined for analysis. The combined data were normalized to identify the differentially expressed genes (DEGs), and GO and KEGG enrichment analyses were performed. Protein-protein interaction (PPI) networks and hub genes between DEGs were identified. We also used the miRWalk database to identify regulatory miRNAs associated with expressions of DEGs. Result We identified 182 DEGs (160 upregulated and 22 downregulated) between Hashimoto's disease patients and the healthy control group. GO analysis showed that DEGs were mostly concentrated in detection of chemical stimulus involved in sensory perception, intermediate filament cytoskeleton, and olfactory receptor activity. KEGG pathway analysis showed that DEGs were mainly related to olfactory transduction. Some members of the KRTAP family and HTR5A, KNG1, DRD3, HTR1D, TAS2R16, INSL5, TAS2R42, and GRM7 are the most important hub genes in the PPI network. In addition, we recognized that OTUD4, LLPH, and ECHDC1 were the most important hub genes in the miRNA-target gene network. Conclusion In this study, a series of bioinformatics analyses of DEGs were performed to identify the key genes and pathways associated with Hashimoto's thyroiditis. These genes and pathways provide a more detailed understanding of the pathogenesis of Hashimoto's disease and provide new ideas for the therapeutic targets of Hashimoto's thyroiditis.
Highlights
Hashimoto’s thyroiditis, known as chronic lymphocytic thyroiditis, is an autoimmune thyroid disease, first described by Hiroshi Hashimoto in 1912
We identified 182 differentially expressed genes (DEGs) in Hashimoto’s Thyroiditis (HT) patients, with a total of 160 upregulated genes and 20 downregulated genes compared with healthy controls
The results showed that there were good differences in these DEGs between HT patients and healthy controls
Summary
Hashimoto’s thyroiditis, known as chronic lymphocytic thyroiditis, is an autoimmune thyroid disease, first described by Hiroshi Hashimoto in 1912. He reported on four patients with chronic thyroid disease, which he called thyroid lymphoma, which was characterized by diffuse lymphocytic infiltration, germinal centers, parenchymal atrophy, fibrosis, and eosinophilic changes in some thyroid follicular cells [1]. The incidence of Hashimoto’s disease is about 0.3-1.5 cases per 1000 people per year [2], and it is gradually increasing. The incidence of women is 5-10 times that of men, and it increases with age (peak age is between 45 and 65 years) [3]. HT is genetically susceptible, many of which are immune-related
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