一种新型的活性硫供体PSCP激活了Keap1-Nrf2信号,并减轻了糖尿病视网膜病变中的线粒体功能障碍
Kexin Li1, Ruiying Ji1, Youbang Chen1
1Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Disease, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Frontiers in endocrinology
|December 3, 2025
概括
糖尿病视网膜病变 (DR) 涉及不太了解的分子驱动因素. 这项研究确定了IDH2和MGST1作为关键标,并表明PSCP通过激活Keap1-Nrf2通路来保护线粒体,为DR提供治疗潜力.
科学领域:
- 眼科医生 眼科 眼科
- 糖尿病学 糖尿病学
- 分子生物学分子生物学
背景情况:
- 糖尿病视网膜病变 (DR) 是糖尿病视力丧失的主要原因.
- 导致DR病变的分子机制尚未完全理解.
- 确定新的治疗点对于管理DR至关重要.
研究的目的:
- 在糖尿病视网膜病变中识别应激响应的分子标.
- 为了研究PSCP的治疗潜力,一个反应性硫供体,在DR.
- 阐明Keap1-Nrf2通路在DR中的作用.
主要方法:
- 来自糖尿病小鼠模型 (1型和2型) 的视网膜转录组数据集的分析.
- 在ARPE-19细胞中使用H2O2或MGO诱导氧化和碳应激.
- 评估线粒体功能,基因表达和抗氧化途径与PSCP和Nrf2抑制剂ML385.5.
主要成果:
- IDH2和MGST1被确定为糖尿病视网膜中的失调的线粒体抗氧化酶.
- 氧化和碳应激损害了线粒体功能和细胞活力,抑制了IDH2和MGST1.
- 通过激活Keap1-Nrf2通路,PSCP治疗恢复了IDH2,MGST1和线粒体动力学,ML385阻止了这种效应.
结论:
- IDH2和MGST1是糖尿病视网膜病变中关键的应激反应性线粒体标.
- 通过激活Keap1-Nrf2通路来保护线粒体完整性,PSCP显示了治疗潜力.
- 准Keap1-Nrf2通路为治疗糖尿病视网膜病变提供了一个有希望的策略.
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