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Thyroid eye disease (TED), also known as Graves’ ophthalmopathy (GO) or thyroid-associated ophthalmopathy (TAO), is an autoimmune orbital disease. The core pathogenic mechanism is immune dysregulation triggered by self-antigens, which activates orbital fibroblasts and leads to pathological changes such as tissue hyperplasia and fibrosis. The clinical manifestations include proptosis and eyelid retraction. MicroRNA (miRNA), as a key factor in post-transcriptional regulation, is widely involved in the occurrence and development of TED. Altered expression profiles of specific miRNAs, such as miR-21, miR-146a, and miR-144-3p, have been observed in clinical samples and in vitro fibroblast models, where they are associated with processes including fibroblast activation, fibrosis, adipogenesis, and inflammation. These findings highlight miRNAs as potential mechanistic targets for further investigation. This review summarizes the pathogenesis of TED and discusses the emerging role of miRNAs based on current clinical and experimental evidence, aiming to provide insights for future research and therapeutic development.
Wang et al. (Mon,) studied this question.
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