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FoxO1,与Notch1一起,促进微质激活,在缺氧下诱导视网膜血管系统的病态变化

Xiyu Wu^1,2, Junbin Liu¹, Haoxian Zhu^1,2

¹Department of Ophthalmology, Guangdong Eye Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Southern Medical University, 106 Zhongshan Er Road, Guangzhou, 510080, China.

Cellular and molecular life sciences : CMLS

|December 21, 2025

概括

缺氧通过Notch1-FoxO1通路激活视网膜微质,在缺血视网膜病变中促进炎症和血管损伤. 针对这一轴为这些疾病提供了潜在的治疗策略.

科学领域:

视网膜免疫学视网膜免疫学
神经炎症是一种神经炎症.
血管生物学血管生物学

背景情况:

微质细胞是视网膜中关键的免疫细胞,参与视网膜病变.
在缺血症期间,Notch信号通路在视网膜微质中的作用尚不清楚.

研究的目的:

调查Notch信号在微质激活和功能中的作用,在缺氧条件下与缺血性视网膜病变相关.
确定特定的分子机制,将缺氧,微质反应和视网膜血管功能障碍联系起来.
评估在临床前模型中针对已识别的途径的治疗潜力.

主要方法:

在视网膜微细胞培养和体内小鼠模型中诱导缺氧 (氧气诱导的视网膜病变).
对微质激活标记物,细胞因子和生长因子表达 (IL-1β,IL-6,TNF-α,FGF2,VEGF,PDGF-β) 的分析.
研究Notch1和FoxO1的核转移及其相互作用.
药理上抑制Notch1和FoxO1通路的作用.

主要成果:

缺氧诱导了微质激活,增加了促炎和促血管的因素.
缺氧触发了视网膜微质中的Notch1-FoxO1核转位.
鉴定出Jagged1-Notch1-FoxO1轴是微质炎症前驱和血管前驱表型的驱动因素.
抑制Notch1或FoxO1在低氧激活的微质细胞和视网膜病变模型中减少了炎症和新血管化.

结论:

诺奇1-FoxO1轴调解微质激活,并在缺氧压力下促进视网膜血管病变.
向Notch1-FoxO1通路代表了管理缺血性视网膜病变中的炎症和新血管化的有前途的治疗策略.

关键词:

在FoxO1中,FoxO1是指FoxO1的类型.氧气过低是因为缺氧.缺血性视网膜病变是一种缺血性视网膜病变.微质细胞中的微质细胞在Notch1路径中.视网膜血管内皮细胞视网膜血管内皮细胞

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