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大脑衍生的细胞外囊泡circusUsp32极化巨细胞,在创伤性脑损伤后引起急性损伤

Jiayuanyuan Fu¹, Jingheng Wu¹, Mengran Du²

¹Huanhu Hospital Affiliated to Tianjin Medical University, Tianjin Medical University, Tianjin 300070, China.

Science advances

|November 26, 2025

概括

创伤性脑损伤 (TBI) 可以通过来自大脑的细胞外囊泡引起损伤. 一种特定的分子,circUsp32,驱动这种炎症,并可能作为TBI后急性损伤 (AKI) 的生物标志物.

科学领域:

神经科学是一个神经科学.
腎臟病學 (nephrology) 是一種醫學專業.
免疫学免疫学免疫学

背景情况:

创伤性脑损伤 (TBI) 可以通过不清楚的脑交叉交谈机制导致急性损伤 (AKI).
来自受伤的大脑组织 (TBI-EVs) 的细胞外囊泡 (EVs) 参与调解这些相互作用.

研究的目的:

阐明TBI-EVs诱导AKI的机制.
确定潜在的分子媒介和生物标志物,涉及到TBI诱导的AKI.

主要方法:

在体外TBI小鼠模型和体外细胞测定被使用.
对TBI-EVs的转录组分析确定了circusp32.
分子测定研究了circUsp32,Socs1和IRF7.7之间的相互作用.

主要成果:

给TBI-EV增加了AKI标志物和促炎性巨细胞极化.
circUsp32在TBI-EV中高度表达,并通过与Socs1相互作用并影响IRF7.7,促进了巨细胞两极分化.
在TBI小鼠中,Knockdown的circusp32缓解了AKI.
circUsp32与潜在的人类AKI生物标志物 (hsa_circ_0044940) 呈现同质性.

结论:

circUsp32通过通过Socs1/IRF7轴促进促炎性巨细胞极化来调解TBI诱导的AKI.
circUsp32是一种潜在的治疗标,也是TBI后AKI的预测生物标志物.

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