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巨细胞的代谢重编程改善了糖尿病引起的微血管功能障碍

Qiu-Yang Zhang¹, Hui-Ying Zhang², Si-Guo Feng²

¹The Affiliated Eye Hospital, Nanjing Medical University, Nanjing, 210000, China; The Fourth School of Clinical Medicine, Nanjing Medical University, Nanjing, 210000, China.

|December 8, 2024

概括

循环RNAcSPECC1通过改变巨细胞代谢,使糖尿病血管疾病恶化. 减少cSPECC1通过恢复巨细胞平衡和减少炎症来保护视网膜血管.

科学领域:

分子生物学分子生物学
免疫学免疫学免疫学
代谢研究研究代谢研究

背景情况:

巨细胞在血管疾病的发展中至关重要,其代谢状态影响疾病的进展.
糖尿病引起的微血管功能障碍是与巨细胞失衡相关的重大健康问题.
人们越来越认识到表观遗传调节,特别是循环RNA的调节,可以维持细胞平衡.

研究的目的:

调查循环RNA介导表观遗传改造在糖尿病诱导的微血管功能障碍期间巨细胞平衡中的作用.
为了确定特定的循环RNAs参与调节巨细胞功能在糖尿病条件.
阐明循环RNAs影响巨细胞-内皮细胞相互作用和血管健康的分子机制.

主要方法:

在糖尿病视网膜和压力巨中识别和定量循环RNA.
功能性研究涉及对巨细胞中已识别的循环RNAs (cSPECC1) 的破坏.
在体外评估巨细胞两极分化 (M1/M2),巨细胞与内皮细胞交叉,以及炎症标志物.
在体内研究评估cSPECC1敲击对糖尿病视网膜病变和血管功能障碍的影响.
探讨cSPECC1与蛋白质 (eIF4A3) 的相互作用及其对基因表达 (GPX2) 和代谢途径 (酸代谢) 的作用的机制研究.

主要成果:

发现一种新型的循环RNA,circSPECC1,在糖尿病压力下在糖尿病视网膜和巨细胞中被上调.
在巨细胞中抑制cSPECC1降低了M1两极分化,改善了巨细胞内皮交叉声,并减少了视网膜炎症.
cSPECC1通过招募eIF4A3,稳定GPX2mRNA,并改变酸代谢来调节GPX2表达.
代谢中间体12-HETE被确定为cSPECC1对巨细胞平衡和血管交叉调节的关键调解者.
外源性12-HETE补充剂逆转了cSPECC1敲击的有益影响,突出了其核心作用.

结论:

在糖尿病的背景下,CircSPECC1是巨细胞介导的血管完整性和炎症的新型调节剂.
针对巨细胞的代谢重编程,特别是通过涉及circSPECC1和12-HETE的途径,为糖尿病血管并发症提供了潜在的治疗策略.
了解circSPECC1的作用为驱动糖尿病微血管功能障碍的表观遗传机制提供了新的见解.

关键词:

循环RNAs是一种循环RNA.糖尿病视网膜病变 - 糖尿病视网膜病变巨细胞的恒常性.代谢重编程是一种代谢重编程.血管功能障碍血管功能障碍

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