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通过ANXA1介导的mTOR/FABP4抑制在狼性炎中驱动抗纤维细胞巨细胞重编程

Juan Tao¹, Qingyu Cheng², Pinjie Zhang³

¹Department of Rheumatology and Immunology, The First Affiliated Hospital of the USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230001, China.

International journal of biological sciences

|March 9, 2026

概括

附录A1 (ANXA1) 蛋白水平随着狼性炎 (LN) 严重程度的增加而增加. 向ANXA1和特定的巨细胞可能为LN患者的纤维化提供新的治疗方法.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

炎症和纤维化是狼性炎 (LN) 的关键病理特征.
素A1 (ANXA1),是髓状细胞中的一种蛋白质,调节炎症和纤维化.
增加的ANXA1表达与LN患者的纤维化严重程度相关.

研究的目的:

为了研究ANXA1和特定的巨细胞子集在狼性炎中纤维化中的作用.
探索巨细胞中的ANXA1信号通路及其对纤维化的影响.
评估基于ANXA1的干预措施在LN的小鼠模型中的治疗潜力.

主要方法:

在LN患者中分析ANXA1表达.
单细胞RNA测序以识别巨细胞子集.
通过FPR2/ALX受体对ANXA1信号传递的机制研究.
用ANXA1-模仿性Ac2-26.2治疗易患狼的小鼠.

主要成果:

脏ANXA1表达在LN患者中升高,与纤维化相关.
一个新的单细胞衍生的Spp1巨细胞子集与profibrotic签名被确定.
通过增强脂肪酸氧化,ANXA1信号促进了抗纤维性巨细胞表型.
在小鼠中,Ac2-26治疗减少了巨细胞驱动的纤维化,脏脂质积累和损伤.

结论:

ANXA1和Anxa1巨细胞在驱动LN的纤维化方面至关重要.
准ANXA1信号提供了一个有前途的治疗策略为狼性炎.

关键词:

附录A1 一,附录A1 一,附录A1 一.脂质代谢重编程脂质代谢重编程狼性炎是一种神经炎症.巨细胞是一个巨细胞.脏纤维化脏纤维化

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