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CD163⁺巨细胞通过互白素-10-10减弱压力过载引起的左心室缩功能障碍和心脏线粒体功能障碍

Wei Ni^1,2, Xiaofeng Ge¹, Yang Liu^1,3

¹School of Medicine, Xiamen Cardiovascular Hospital, Xiamen University, Jinshan Road 2999, Xiamen, 361015, China.

Basic research in cardiology

|May 9, 2025

概括

CD163阳性巨细胞通过通过IL-10维持线粒体功能来保护心力衰竭. 耗尽这些细胞会恶化心脏功能障碍,突出显示它们在压力过载条件下的治疗潜力.

科学领域:

心血管生物学心血管生物学
免疫学免疫学免疫学
线粒体医学线粒体医学

背景情况:

巨细胞枯竭会使心力衰竭恶化,但子组的作用尚不清楚.
在心力衰竭中,CD163阳性 (CD163+) 巨细胞的特定功能需要阐明.

研究的目的:

研究CD163+巨细胞在压力过载引起的心力衰竭中的作用.
确定潜在的机制,特别是互白素-10 (IL-10) 的参与.

主要方法:

通过横向大动脉收缩 (TAC) 诱导压力过载在野生型 (WT) 和CD163缺乏 (Cd163-/-) 的小鼠中.
通过RNA测序和传输电子显微镜评估心脏功能,使用心声学和心脏组织分析.
评估IL-10水平和IL-10补充剂的影响.

主要成果:

Cd163-/-小鼠显示TAC诱导的左心室功能障碍和线粒体损伤加剧.
心脏巨细胞在TAC后增加了CD163+比例,在Cd163-/-小鼠中减少了IL-10.
在Cd163-/-小鼠中,补充IL-10可挽救心脏功能,改善线粒体健康.
在高血压患者中,较低的IL-10水平与心力衰竭风险相关.

结论:

CD163+巨细胞对压力过重引起的心力衰竭产生保护作用.
这种保护通过一种依赖IL-10的途径进行介导,从而保持线粒体功能.
向CD163+巨细胞或IL-10代表了心力衰竭的潜在治疗策略.

关键词:

CD163 是一个CD163 CD163 是一个CD163 功能障碍的线粒体功能障碍的线粒体心脏衰竭是因为心脏衰竭.介质蛋白-10 介质蛋白-10 是一种压力过载的压力过载

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