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在糖尿病视网膜病变中,FXR通过调节cGAS/STING通路来抑制穆勒细胞激活

Zi-Li Wang¹, Xin-Yu Zhang¹, Cheng-Ye Tan¹

¹Department of Ophthalmology, The Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi People's Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi, China.

The FEBS journal

|February 11, 2025

概括

法尔内索伊德X受体 (FXR) 激活通过减少视网膜炎症和线粒体功能障碍来保护糖尿病视网膜病变 (DR). 准FXR为DR治疗提供了一个有前途的治疗策略.

科学领域:

眼科医生眼科眼科
内分泌学在内分泌学.
细胞生物学细胞生物学

背景情况:

糖尿病视网膜病变 (DR) 涉及视网膜炎症和神经血管退行.
穆勒质细胞是视网膜平衡和神经炎症的关键.
法尔内索伊德X核受体 (FXR) 调节代谢和炎症途径.

研究的目的:

调查FXR在糖尿病视网膜病变 (DR) 中的作用.
为了确定FXR激活是否可以减轻DR进展.
为了阐明FXR在DR的保护作用的潜在机制.

主要方法:

在Sprague-Dawley大鼠中利用了链毒素 (STZ) 诱导的糖尿病视网膜病变模型.
用先进的糖化终产物 (AGEs) 或高葡萄糖/棕酸盐 (HG+PA) 处理的人类穆勒质细胞.
评估了FXR表达,炎症标志物,线粒体功能和cGAS/STING通路.

主要成果:

在DR模型中,FXR表达被下调.
FXR激活抑制了穆勒细胞炎症并减轻了DR进展.
通过ATF4/NRF1调节TFAM,抑制mtDNA释放和cGAS/STING激活,FXR改善了线粒体功能障碍.
FXR的淘汰扭转了这些保护效应.

结论:

FXR激活显示出对糖尿病视网膜病变的显著保护作用.
通过TFAM/ATF4/NRF1通路抑制炎症并恢复线粒体功能,FXR可以减轻DR.
准FXR为管理糖尿病视网膜病变提供了潜在的治疗途径.

关键词:

在ATF4/NRF1/TFAM中使用.在 FXR 和 FXR 之间.cGAS/STING的使用情况.糖尿病视网膜病变糖尿病视网膜病变线粒体功能障碍线粒体功能障碍

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