微质-内皮交叉对话通过重塑炎症微环境来调节糖尿病诱导的视网膜血管功能障碍
Shuai Ben1,2,3, Yan Ma4,5, Yun Bai6
1Department of Ophthalmology, Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200080, China.
iScience
|February 28, 2024
概括
糖尿病视网膜病变涉及脑免疫细胞和血管细胞之间的炎症交叉声. 殖民地刺激因子1 (CSF1) 和它的受体 (CSF1R) 途径失调驱动微质变化和血管生长在这种情况下.
科学领域:
- 神经免疫学 神经免疫学
- 血管生物学 血管生物学
- 眼科医生 眼科 眼科
背景情况:
- 神经质细胞和内皮细胞 (ECs) 之间的炎症驱动的交叉声是血管疾病的关键.
- 糖尿病诱导的微血管功能障碍,特别是糖尿病视网膜病变 (DR) 的特定炎症机制尚未完全理解.
研究的目的:
- 使用单细胞RNA测序阐明糖尿病视网膜病变 (DR) 的转录格局.
- 在糖尿病的背景下,研究微质和EC之间的细胞间交叉声.
- 确定关键的分子参与者和涉及DR病变发生的途径.
主要方法:
- 单细胞RNA测序 (scRNA-seq) 的视网膜细胞.
- 微质细胞和内皮细胞 (ECs) 的转录基因分析.
- 研究细胞间通信通路,重点关注CSF1/CSF1R信号传输.
主要成果:
- scRNA-seq在DR中发现了两个不同的微质子群和三个EC群.
- 糖尿病引起的微质-EC交叉声主要涉及炎症反应和血管发育.
- 殖民地刺激因子1 (CSF1) 和它的受体 (CSF1R) 信号传递对于早期细胞分化至关重要,并且在增殖性DR中失调.
- ECs分泌CSF1,激活微质中的CSF1R信号,通过MAPK通路激活促进分化,炎症因子分泌和血管生成.
结论:
- 对CSF1/CSF1R通路的失调是糖尿病视网膜病变的一个关键机制.
- 已确定的微质-EC交叉通路有助于DR的炎症和异常血管生成.
- 准CSF1/CSF1R-MAPK轴可能为管理DR提供治疗策略.
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