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tRF-AspGTC 通过控制TRIM29介导的Galactin-3 Ubiquitination来促进内动脉瘤的形成

Chao Wang¹, Bing Yu, Han Zhou²

¹Department of Neurosurgery and Institute for Translational Medicine, The Affiliated Hospital of Qingdao University, Qingdao 266000, People's Republic of China.

Research (Washington, D.C.)

|January 8, 2025

概括

转移RNA衍生片段AspGTC (tRF-AspGTC) 通过改变血管细胞和炎症来促进内动脉瘤 (IA) 的形成. 循环的tRF-AspGTC显示了IA的诊断潜力.

科学领域:

分子生物学分子生物学
遗传学是一个遗传学.
心血管研究研究心血管研究

背景情况:

转移RNA衍生小RNA (tRFs) 是基因表达的新兴调节者.
它们在脑血管疾病,特别是内动脉瘤 (IA) 中的作用在很大程度上是未知的.

研究的目的:

调查tRF-AspGTC在IA病变发生中的作用和机制.
评估tRF-AspGTC作为IA的诊断生物标志物.

主要方法:

在人类和小鼠IA组织中对tRF-AspGTC表达的定量分析.
在体外和体外实验以阐明tRF-AspGTC的分子机制.
针对诊断潜力的循环外体tRF-AspGTC的分析.

主要成果:

在IA组织中,tRF-AspGTC被显著上调.
tRF-AspGTC通过诱导血管光滑肌细胞表型切换,MMP9表达,氧化应激和炎症来促进IA.
tRF-AspGTC通过抑制TRIM29无化,激活TLR4/MyD88/NF-κB通路来稳定加勒-3的作用.
循环外体tRF-AspGTC作为一个敏感的诊断标记物和IA的独立风险因素.

结论:

tRF-AspGTC是IA形成和进展的关键驱动力.
tRF-AspGTC代表了一个潜在的诊断生物标志物和内动脉瘤的治疗标.

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