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RIPK3编排与痕相关的巨细胞功能障碍,驱动肺纤维化

Tao Yang¹, Xiao Li¹, Shuyue Lei¹

¹School of Pharmacy, University of Chinese Academy of Sciences, Beijing, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|February 19, 2026

概括

受体相互作用蛋白激酶3 (RIPK3) 通过控制巨细胞代谢来调节肺纤维化,独立于细胞死亡. 准这种途径为异形性肺纤维化 (IPF) 提供了潜在的治疗策略.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
代谢过程中的代谢.

背景情况:

异常性肺纤维化 (IPF) 涉及异常组织重塑和免疫系统功能障碍.
受体相互作用蛋白激酶3 (RIPK3) 已知其在亡中的作用,但其在纤维化中的非亡功能尚不清楚.

研究的目的:

为了研究RIPK3在肺纤维化中的非尸性功能.
确定RIPK3在纤维化期间调节巨细胞功能和新陈代谢中的作用.

主要方法:

在IPF患者和小鼠中分析RIPK3表达.
产生和分析巨细胞特异性RIPK3淘汰小鼠.
蓝素诱导的肺纤维化模型.
单细胞RNA测序. 一个单细胞RNA测序.
在体外分化和痕相关巨细胞 (SAM) 的功能分析.

主要成果:

RIPK3在IPF上升调节,并在巨细胞中丰富.
巨细胞特异性RIPK3淘汰小鼠对白血素诱导的纤维化表现出耐药性.
RIPK3调节SAM及其亲纤维功能.
在SAM中RIPK3缺乏抑制了通过AKT-mTOR途径将氨酸转化为聚胺的转化,减少了亲纤维聚胺的积累.

结论:

在肺纤维化中,RIPK3具有独特的,不依赖死细胞的免疫代谢作用.
通过影响SAMS,RIPK3在纤维化位中起到关键的代谢调节作用.
针对RIPK3介导的免疫代谢轴为IPF提供了潜在的治疗策略.

关键词:

在IPF中,IPF是IPF.在RIPK3中使用RIPK3.萨姆导弹 (SAMS) 是一种对空导弹.SPP1 SPP1 这是一个很好的选择.阿尔金因的代谢过程

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