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.

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桥本甲状腺炎相关基因的综合分析

客观的。桥本甲状腺炎又称慢性淋巴细胞性甲状腺炎，是一种常见的自身免疫性甲状腺炎，多发生于中青年女性。早期可表现为甲亢；随着疾病的进展，可能会出现甲状腺功能减退症。研究表明遗传、环境、自身免疫等多种因素参与发病，但具体机制尚不清楚。本研究试图寻找桥本甲状腺炎的关键基因和潜在的分子机制，为桥本甲状腺炎的治疗靶点提供新思路。方法。从GEO数据库下载GSE138198和GSE54958，并将两个数据集合并进行分析。对组合数据进行归一化以确定差异表达基因 (DEG)，并进行 GO 和 KEGG 富集分析。确定了 DEG 之间的蛋白质-蛋白质相互作用 (PPI) 网络和中心基因。我们还使用 mirWalk 数据库来识别与 DEG 表达相关的调控 miRNA。结果。我们在桥本氏病患者和健康对照组之间确定了 182 个 DEG（160 个上调和 22 个下调）。GO分析表明DEG主要集中于检测涉及感觉知觉、中间丝细胞骨架和嗅觉受体活性的化学刺激。KEGG通路分析显示DEGs主要与嗅觉转导相关。KRTAP 家族的一些成员以及 HTR5A、KNG1、DRD3、HTR1D、TAS2R16、INSL5、TAS2R42 和 GRM7 是 PPI 网络中最重要的枢纽基因。此外，我们认识到 OTUD4、LLPH 和 ECHDC1 是 miRNA 靶基因网络中最重要的枢纽基因。结论。在本研究中，对 DEG 进行了一系列生物信息学分析，以确定与桥本甲状腺炎相关的关键基因和通路。这些基因和通路让我们更加详细地了解桥本氏病的发病机制，并为桥本氏甲状腺炎的治疗靶点提供新思路。