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与肥胖相关的巨细胞通过传播线粒体分裂来决定脂肪干细胞铁和内脏脂肪功能障碍

Yan Tao¹, Jinhao Zang¹, Tianci Wang¹

¹Key Laboratory of Infection and Immunity of Shandong Province, Department of Immunology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, China.

Nature communications

|August 14, 2025

概括

巨细胞中TIPE2的丧失通过促进脂肪干细胞铁亡,使肥胖症恶化. 在巨细胞中恢复TIPE2可以通过防止细胞死亡来防止代谢障碍.

科学领域:

免疫学免疫学免疫学
代谢疾病代谢疾病
细胞生物学细胞生物学

背景情况:

致病性肥胖导致脂肪干细胞 (ASC) 短缺,破坏内脏脂肪组织 (VAT) 恒温.
巨细胞和TNF-α诱导蛋白8-like 2 (TIPE2) 在VAT巨细胞-ASC交叉和ASC缺陷中的作用尚不清楚.

研究的目的:

研究TIPE2在VAT巨细胞中的功能及其在巨细胞-ASC交叉声调中的作用.
探索向巨细胞TIPE2作为治疗肥胖相关疾病的治疗策略的潜力.

主要方法:

利用了因饮食引起的肥胖症的雄性小鼠模型.
在增值税巨中操纵TIPE2表达.
分析了ASC铁,线粒体功能和通过外体细胞的细胞间通信.

主要成果:

增值税巨细胞中的TIPE2缺乏促进了ASC铁,加剧了肥胖和代谢障碍.
宏细胞特异性TIPE2恢复纠正了这些代谢障碍.
缺少TIPE2的巨细胞诱导了线粒体碎片化和减少了外体,导致ASC中的ROS和Fe2+过载,导致铁亡.

结论:

巨细胞TIPE2抑制IP3R-Ca2+-Drp1轴,防止过度的线粒体裂变,并保护ASCs免受铁亡.
明显的与肥胖相关的巨细胞决定ASC铁死.
巨 TIPE2 是肥胖和相关代谢疾病的潜在治疗标.

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