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CTRP6作为抗炎M2巨细胞两极分化的负调节剂

Jeevotham Senthil Kumar¹, Emma Kempton¹, Muhammad Zubair Mehboob¹

¹Department of Biochemistry and Molecular Biology, Oklahoma State University, Stillwater, OK, USA.

Immunometabolism (Cobham, Surrey)

|October 29, 2025

概括

与C1q/TNF相关的蛋白6 (CTRP6) 抑制了肥胖症中抗炎M2巨分化. 这种蛋白质阻碍了炎症的解决,加剧了脂肪组织的炎症,并导致肥胖的病理生理学.

科学领域:

生物化学生物化学
免疫学免疫学免疫学
代谢疾病代谢疾病

背景情况:

脂肪组织中由巨细胞驱动的慢性低度炎症是肥胖的核心原因.
与C1q/TNF相关的蛋白6 (CTRP6) 是脂肪组织炎症的关键调节者.
在肥胖期间,CTRP6表达在脂肪组织巨细胞中升高,抑制M2极化.

研究的目的:

调查CTRP6在调节肥胖症中巨细胞极化中的作用.
确定CTRP6对M1和M2巨细胞极化标记物和信号通路的影响.
为了验证细胞系和初级巨细胞的发现.

主要方法:

使用RAW264.7细胞系和初级骨髓衍生的巨细胞 (BMDMs) 分化M1和M2巨细胞.
使用的脂聚糖 (LPS) +干扰素- (IFNγ) 用于M1偏振和介质素 (IL) -4 用于M2偏振.
评估了重组CTRP6蛋白对巨细胞极化标记物,信号通路 (STAT6,ERK1/2) 和线粒体活性的影响.

主要成果:

在原始巨细胞中,CTRP6上调的M1标记物 (Tnf,No2) 和下调的M2标记物 (Mrc1,Pparg).
通过抑制STAT6信号传递和缓解ERK1/2抑制,CTRP6抑制了IL-4诱导的M2极化.
CTRP6 损害了线粒体活动,促进了糖解,并证实了BMDMs中的效果.

结论:

CTRP6通过抑制M2极化来阻碍炎症的解决,即使存在IL-4.
在BMDM中升级的CTRP6有助于肥胖的脂肪组织炎症.
在肥胖病理生理学中,CTRP6是慢性炎症的重要驱动因素.

关键词:

在CTRP6中使用.M2巨细胞的两极分化脂肪组织的脂肪组织.这是一种炎症炎症炎症炎症.负调节器是一个负调节器.

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