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在代谢障碍中通过TSHR信号传导对TSH介导的巨细胞线粒体功能障碍进行机制性洞察

Yuhan Zhang¹, Hanyu Wang¹, Mengfei Fu²

¹Department of Endocrinology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Hubei Provincial Clinical Research Center for Diabetes and Metabolic Disorders, Wuhan, China.

Free radical biology & medicine

|July 22, 2025

概括

巨细胞中的甲状腺刺激激素受体 (TSHR) 在亚临床甲状腺功能低下症中驱动代谢功能障碍. 通过Cyclophilin D (CypD) 抑制TSHR信号传递可以改善线粒体功能并减少炎症.

科学领域:

内分泌学在内分泌学.
免疫学免疫学免疫学
代谢障碍代谢障碍代谢障碍

背景情况:

甲状腺刺激激素受体 (TSHR) 在巨细胞中对脂肪组织代谢障碍的作用尚未完全理解.
亚临床甲状腺功能低下症 (SCH) 与代谢并发症有关,但涉及巨细胞TSHR的潜在机制尚不清楚.

研究的目的:

调查巨TSHR在SCH期间代谢和炎症疾病的发展中的功能.
阐明巨细胞中TSHR信号传递影响脂肪组织恒常性的分子机制.

主要方法:

产生巨细胞特异性TSHR淘汰赛小鼠 (LysM-Cre Tshr) 和使用甲基马诱导的SCH.
使用葡萄糖/胰岛素耐受性测试,组织学和分子分析评估代谢和炎症表型.
检查了线粒体功能和巨细胞的两极分化在体外和体内,专注于TSH刺激和Cyclophilin D (CypD) 抑制.

主要成果:

大细胞TSHR缺失减弱了SCH诱导的胰岛素抵抗,炎症和脂肪细胞缩.
通过TSHR-依赖的线粒体功能障碍,包括mPTP过度激活和氧化应激,TSH促进了前炎性巨分化.
CypD调解了TSH诱导的线粒体功能障碍,其与环素A (CsA) 的抑制逆转了这些 in vitro 和 in vivo 的效应.

结论:

巨细胞中TSHR信号加剧脂肪组织功能障碍SCH通过破坏线粒体平衡和促进亲炎性两极化.
TSHR-CypD轴代表了管理与SCH相关的代谢障碍的潜在治疗标.

关键词:

这就是CypDD.亚临床的甲状腺功能低下症甲状腺刺激激素激素激发甲状腺刺激激素.

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