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Role of thyroid hormone in an experimental model of atherosclerosis: the potential mediating role of immune response and autophagy

期刊

ENDOCRINE JOURNAL
卷 -, 期 -, 页码 -

出版社

JAPAN ENDOCRINE SOC
DOI: 10.1507/endocrj.EJ22-0177

关键词

Thyroid hormone; Thyroid-stimulating hormone (TSH); Immune response; Atherosclerosis; Autophagy

资金

  1. KAKENHI from the Japan Society for the Promotion of Science [19K17981, 21K08772]

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This article provides an overview of the dynamic interactions between thyroid hormone status and immune response in the pathogenesis of atherosclerosis. The role of macrophages and T-lymphocytes as important determinants in the initiation and development of atherosclerosis is highlighted. The study also suggests that thyroid hormone-mediated autophagy could serve as a novel therapeutic approach for atherosclerosis.
Accumulating evidence has revealed that several conditions related to abnormal thyroid hormone status, such as dyslipidemia, hypertension, or hypercoagulable state, can exacerbate atherosclerotic vascular disease. Thyroid hormone effects on vascular smooth muscle cells and endothelial cells have also been studied extensively. However, only limited information is available on thyroid hormone-mediated immune response in current review articles on the pathophysiology of atherosclerosis. This report thus presents an overview of the recent advances in the understanding of the dynamic interactions taking place between thyroid hormone status and immune response in the pathogenesis of atherosclerosis. In particular, we focus on macrophages and T-lymphocytes, which have been recognized as important determinants for the initiation and development of atherosclerosis. Numerous studies have revealed the role of autophagy in immune cells produced in atherosclerosis. In addition, thyroid hormones induce autophagy in several cells and tissues, such as liver, skeletal muscles, lungs, and brown adipose tissue. Our research group, among others, have reported different targets of thyroid hormone-mediated autophagy, including lipid droplets (lipophagy), mitochondria (mitophagy), and aggregated proteins (aggrephagy). Based on these findings, thyroid hormone-mediated autophagy could serve as a novel therapeutic approach for atherosclerosis. We also consider the limitations of the current murine models for studies on atherosclerosis, especially in relation to low-density lipoprotein-cholesterol driven atherosclerotic plaque.

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