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巨细胞MRC2缺陷通过降低CD147调节的TNF-α产生来缓解HFD诱导的MASLD

Hui-Ru Kuo^1,2, Kwei-Yan Liu², Hsin-Ying Clair Chiou^3,4

¹Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.

JHEP reports : innovation in hepatology

|December 9, 2025

概括

巨细胞上的C2型曼诺糖受体 (MRC2) 通过激活CD147信号和TNF-α释放,促进代谢功能障碍相关的脂肪性肝病 (MASLD). 缺乏MRC2可缓解肝脏肥胖和炎症,这表明MRC2是MASLD的治疗点.

科学领域:

肝病学肝病学是一种肝病学.
免疫学免疫学免疫学
代谢疾病代谢疾病

背景情况:

与代谢功能障碍相关的脂肪性肝病 (MASLD) 的机制尚未完全理解,其中涉及慢性炎症.
曼诺酶受体C型2 (MRC2) 正在研究其在MASLD病原发生中的潜在作用.

研究的目的:

调查MRC2对MASLD发展的贡献.
阐明涉及巨细胞相关炎症的潜在分子机制.

主要方法:

使用的野生型和MRC2缺乏的小鼠被食高脂肪饮食 (HFD).
使用了用棕酸刺激的初级肝细胞和骨髓衍生的巨细胞.
评估了MRC2缺乏和CD147-NF-κB信号对肝硬化和TNF-α产生的影响.

主要成果:

患者和小鼠中MRC2水平升高与MASLD严重程度相关.
缺乏MRC2的小鼠表现出减少HFD诱导的体重增加和肥胖症.
巨细胞衍生的MRC2通过MRC2-CD147复合体促进了肥胖症,损害了NF-κB信号传递和TNF-α释放.

结论:

大菌MRC2通过MRC2-CD147复合体驱动HFD养小鼠的肝硬化症.
向巨细胞MRC2-CD147复合体为MASLD提供了一个新的治疗策略.

关键词:

CD147 是一个CD147 CD147 是一个CD147 脂质代谢脂质代谢是一种巨细胞是一个巨细胞.曼诺酶受体C型2类型的受体与代谢功能障碍相关的脂肪性肝病.

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