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在糖尿病视网膜病变中具有双重亲血管和亲纤维的MARCO+微细胞表型

Qinyuan Gu¹, Xiying Mao¹, Jingyi Xu¹

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

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

|September 1, 2025

概括

在多发性糖尿病视网膜病变中,MARCO+ 微会促进血管生成和纤维化. 用PolyG向这些细胞减少了眼部疾病的进展,这表明MARCO+微质是治疗点.

科学领域:

眼科眼科
免疫学
血管生物学

背景情况:

增殖性糖尿病视网膜病变 (PDR) 涉及视网膜新血管化和纤维化,导致视力丧失.
抑制血管化和纤维化对于治疗PDR至关重要.
在PDR中,纤维血管膜 (FVM) 是病理变化的关键部位.

研究的目的:

研究特定微质子群在PDR中的作用.
确定眼动血管和纤维性疾病的潜在治疗点.

主要方法:

来自PDR患者的FVM单细胞测序.
在体外研究中使用用糖性白蛋白 (GA) 治疗的BV2细胞.
使用氧气诱导视网膜病变 (OIR) 和胆管新血管化 (CNV) 的小鼠模型 (WT和MARCO-/-) 的体内研究.
下一代测序用于分析信号通路.
使用PolyG对MARCO+微细胞进行药理抑制.

主要成果:

在PDR FVM中发现了具有亲血管性和亲纤维性作用的MARCO+微子群.
在BV2细胞中,GA对MARCO表达的上调取决于剂量.
在WT小鼠中,MARCO+微质积累增强了视网膜血管生成和纤维生成,但在MARCO-/-小鼠中没有.
TLR4/ NF- kB信号通路的激活与MARCO+微质表达的增加有关.
在小鼠模型中,PolyG治疗减少了血管生成和纤维生成.

结论:

在促进眼球血管生成和纤维生成方面,MARCO+ 微质具有重要作用.
使用像PolyG这样的药物准MARCO+微质细胞显示出对PDR和类似疾病的治疗潜力.
在眼部血管性和纤维性疾病中,MARCO+微质是有前途的治疗点.

关键词:

马可蛋白质糖尿病视网膜病变纤维化微质细胞新血管化

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