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在糖尿病视网膜病变中,微质细胞的STING免疫激活会加重神经血管单元损伤

Hong-Ying Li¹, Jingfan Wang¹, Tianhao Xiao¹

¹Department of Ophthalmology, The First Afliated Hospital with Nanjing Medical University, Nanjing Medical University, Nanjing, China.

Free radical biology & medicine

|March 30, 2025

概括

微质中的干扰素基因 (STING) 刺激器通过激活神经炎症来驱动糖尿病视网膜病变 (DR). 在微质中抑制STING为DR治疗和预防失明提供了潜在的治疗策略.

科学领域:

眼科医生眼科眼科
神经科学是一个神经科学.
免疫学免疫学免疫学

背景情况:

糖尿病视网膜病变 (DR) 通过神经炎症和新血管化引起失明,破坏视网膜神经血管单元 (NVU).
微质激活与DR病原发生有关,但其潜在机制尚未完全理解.

研究的目的:

调查干扰素基因刺激器 (STING) 在微质激活中的作用及其对DR的贡献.
探索STING抑制作为DR的潜在治疗点.

主要方法:

使用氧气诱导视网膜病变 (OIR) 和链毒素 (STZ) 诱导的糖尿病小鼠模型.
在微质和视网膜组织中检查了STING表达.
在高葡萄糖和缺氧条件下,研究了BV2细胞中的STING激活.
评估了STING抑制 (药理和遗传) 对微质激活,内皮细胞行为和视网膜质细胞 (RGC) 生存的影响.
在体内评估了AAV介导的STING抑制的治疗潜力.

主要成果:

在OIR和STZ小鼠的纤维血管膜和视网膜内的微质中观察到升级的STING.
高葡萄糖和缺氧诱导了BV2细胞中的STING上调,与线粒体功能障碍和mtDNA释放有关.
在微质中抑制STING阻止了它们的激活和两极分化.
缺少STING的微质细胞逆转了内皮的益血管性行为,并保护RGCs免受氧化应激.
在OIR和STZ小鼠中,内AAV-STING的使用改善了视网膜神经血管病理.

结论:

线粒体DNA (mtDNA) 释放调解了微质细胞的STING免疫激活,加剧了DR中的NVU损伤.
向微质细胞中的STING代表了管理糖尿病视网膜病变和预防视力丧失的有希望的治疗策略.

关键词:

糖尿病视网膜病变 - 糖尿病视网膜病变神经炎症是一种神经炎症.神经血管单位神经血管单位氧化应激是一种氧化应激.刺痛是一种刺痛.

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