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自身免疫性甲状腺疾病的分子机制。

Molecular Mechanisms in Autoimmune Thyroid Disease.

机构信息

Metabolic Diseases Study Group, Department of Internal Medicine, Universidad del Cauca, Carrera 6 Nº 13N-50, Popayán 190001, Colombia.

出版信息

Cells. 2023 Mar 16;12(6):918. doi: 10.3390/cells12060918.

Abstract

The most common cause of acquired thyroid dysfunction is autoimmune thyroid disease, which is an organ-specific autoimmune disease with two presentation phenotypes: hyperthyroidism (Graves-Basedow disease) and hypothyroidism (Hashimoto's thyroiditis). Hashimoto's thyroiditis is distinguished by the presence of autoantibodies against thyroid peroxidase and thyroglobulin. Meanwhile, autoantibodies against the TSH receptor have been found in Graves-Basedow disease. Numerous susceptibility genes, as well as epigenetic and environmental factors, contribute to the pathogenesis of both diseases. This review summarizes the most common genetic, epigenetic, and environmental mechanisms involved in autoimmune thyroid disease.

摘要

获得性甲状腺功能障碍最常见的原因是自身免疫性甲状腺疾病,这是一种具有两种表现型的器官特异性自身免疫性疾病:甲状腺功能亢进症(格雷夫斯病)和甲状腺功能减退症(桥本甲状腺炎)。桥本甲状腺炎的特点是存在针对甲状腺过氧化物酶和甲状腺球蛋白的自身抗体。同时,在格雷夫斯病中发现了针对 TSH 受体的自身抗体。许多易感基因以及表观遗传和环境因素都促成了这两种疾病的发病机制。本综述总结了自身免疫性甲状腺疾病中最常见的遗传、表观遗传和环境机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9844/10047067/502731295ce7/cells-12-00918-g001.jpg

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