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由OGT介导的O-GlcNAcylation通过向IRF1来调节心力衰竭中的巨细胞两极分化

Guoqiang Jing¹, Yuhong Ma²

¹Department of Cardiovascular Medicine, The Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia, 010050, China.

BMC cardiovascular disorders

|December 30, 2024

概括

沉默与O相关的N-乙糖胺 (O-GlcNAcylation) 酶OGT将巨细胞转移到抗炎状态,缓解心力衰竭 (HF). 这表明O-GlcNAcylation是高频率的潜在治疗标.

科学领域:

生物化学生物化学
免疫学免疫学免疫学
心血管医学心血管医学

背景情况:

心力衰竭 (HF) 是一个全球性健康问题,死亡率高.
巨细胞炎症对HF病变产生有显著的贡献.
O-GlcNAcylation是一种后翻译性修饰,影响各种细胞过程.

研究的目的:

调查O-GlcNAcylation在心力衰竭中的作用.
确定O-GlcNAcylation对高频的巨细胞极化的影响.

主要方法:

利用脂聚糖 (LPS) 诱导Raw264.7细胞中的亲炎性巨细胞.
通过横向大动脉收缩 (TAC) 生成高频小鼠模型.
评估了使用qPCR和流细胞计在OGT淘汰或IRF1过度表达后的巨细胞极化;通过生物信息学,co-IP,IP和西部涂抹分析了机制.

主要成果:

在LPS治疗的细胞中观察到高的O-GlcNAcylation和OGT水平.
消灭OGT抑制了促炎性并促进了抗炎性巨细胞两极分化.
通过抑制IRF1 O-GlcNAcylation在Ser283.3,OGT沉默缓解了TAC诱导的心脏功能障碍和纤维化.

结论:

OGT沉默促进了巨细胞两极分化向抗炎性表型的转变,从而改善了HF.
这种有益的效果是通过IRF1.1的O-GlcNAcylation进行介导的.
O-GlcNAcylation成为心力衰竭治疗的有前途的治疗策略.

关键词:

心脏衰竭是因为心脏衰竭.在 IRF2 中, IRF2 是 IRF2 的类型.脂聚糖类糖化物脂聚糖类糖化物这是一种O-GlcNAcylation.其他 OGT 产品.支持/抗炎性巨细胞.

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