数据日期 2026-10-29 · 生成时间 2026-10-29 06:03
证据级别：摘要级。本条依据 PubMed 结构化摘要与元数据撰写，付费墙全文未获取、未逐节核验，本站未做任何数值推算补全。
研究问题
Endothelial cell dysfunction has been identified as a major risk factor for atherosclerosis.
方法
The long non-coding RNA (LncRNA) RNA component of mitochondrial RNA processing endoribonuclease (RMRP) has been detected in mitochondria and is closely associated with inflammation and autophagy.
核心结论
However, the role of the lncRNA RMRP in endothelial cell injury and its potential molecular mechanisms remain unclear.；Mouse aortic endothelial cells (MAECs) were treated with oxidised low-density lipoprotein (ox-LDL).；Changes in cell viability, proinflammatory cytokine levels, mitophagy, and mitochondrial membrane potential in MAECs were assessed to investigate the effects of lncRNA RMRP and protein kinase B (AKT3) on endothelial injury.；Knockdown and overexpression experiments were performed to determine the effects of lncRNA RMRP, polypyrimidine tract-binding protein 1 (PTBP1), and AKT3 on MAECs stimulated with ox-LDL. ‖ 结论：Overexpressed lncRNA RMRP targets AKT3 by recruiting PTBP1, thus activating the PI3K/AKT pathway to mediate mitophagy and promote the progression of atherosclerosis.
局限
未能获取全文，具体设计细节、失访与统计学处理无法核验。
对本项目的价值
★★★☆☆ 血管老化提供可影像量化、可短期读取的中间终点，适合做机制到临床的桥接。
原文题录
- 英文标题：M6A-modified lncRNA RMRP facilitates mitophagy and promotes ox-LDL-induced endothelial cell injury by interacting with PTBP1 and activating the PI3K/AKT pathway.
- 期刊与标识：Biochim Biophys Acta Gene Regul Mech · PMID 42946245 · DOI 10.1016/j.bbagrm.2026.195190**
B 级证据分级：B 级（同行评议临床前研究，主要为动物模型）
本文核心结论来自动物模型或体外细胞学，属临床前证据，不能外推至人体。「延长健康寿命」「改善功能」等表述在小鼠中的意义，与人类临床结局之间仍有距离。
关于本文的文献来源：本站依据 IMA 知识库「五刊监控·深度文献卡片」（SOP §4.2 摘要级）撰写，依据期刊公开摘要与 PubMed 元数据；付费墙全文未获取之处已标注「待补全文」，未做任何数值推算补全。