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Nrf3-Trim5轴在血管光滑肌肉细胞功能障碍和新极度增生症中的新型作用

Qishan Chen^1,2, Shasha Sun¹, Zhenning Shi^1,2

¹Department of Cardiology, Institute for Developmental and Regenerative Cardiovascular Medicine, Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine, China.

Cardiovascular research

|May 16, 2025

概括

核因素红色素2相关因子3 (Nrf3) 通过激活Trim5基因,促进血管光滑肌细胞 (VSMC) 功能障碍和动脉重塑,驱动新极度增生症 (NIH). 抑制这种Nrf3-Trim5通路为血管疾病提供了一种新的治疗策略.

科学领域:

血管生物学血管生物学
分子医学是分子医学.
细胞信号传输细胞信号传输

背景情况:

新极性增生症 (NIH) 是血管疾病 (如动脉样硬化和静脉缩) 中的一个关键病理过程,经常导致缺血性并发症.
血管光滑肌细胞 (VSMC) 功能障碍是NIH的核心,但治疗目标仍然有限.
核因子红色素2相关因子3 (Nrf3) 已涉及VSMC分化,但其在NIH中的作用基本上是未知的.

研究的目的:

调查Nrf3在VSMC功能障碍和NIH引起的损伤中的功能作用.
阐明Nrf3在血管改造中的作用背后的分子机制.
评估在NIH中准Nrf3通路的治疗潜力.

主要方法:

在人类动脉样和转录组数据集中对Nrf3表达的分析.
全球 (Nrf3-/-) 和VSMC特定 (Nrf3ΔSMC) Nrf3淘汰赛小鼠模型的生成和利用.
分子分析以确定Nrf3下游目标和调节途径.
评估Nrf3抑制在一个猪大动脉支架模型的血管改造.

主要成果:

人类动脉样硬化血管中Nrf3表达升高,与NIH正相关.
细胞内膜网膜 (ER) 的压力会通过ATF4.4诱导Nrf3的表达.
Nrf3促进VSMC的增殖,迁移和炎症;它的缺失减轻了受伤引起的NIH.
Nrf3上调调节三方动机含有5 (Trim5) 的表达,增强自和促进VSMC功能障碍.
在淘汰赛小鼠中恢复 Nrf3 或 Trim5 挽救的动脉表型.
在猪模型中,Nrf3抑制显著降低了缩.

结论:

Nrf3是VSMC功能障碍和NIH引起的损伤的关键调解者.
Nrf3通过转录激活Trim5来促进NIH,Trim5驱动自和血管重塑.
针对Nrf3-Trim5信号轴为NIH相关的血管疾病提供了一个有前途的治疗策略.

关键词:

自自是一种自的过程.细胞迁移细胞迁移细胞的增殖细胞的增殖.细胞内膜网膜应激压力这是新亲密的.新极端的增生症.核因子3 (Nrf3) 与红色素2相关的核因子3 (Nrf3)猪大动脉复缩的情况血管造形术后的静脉复缩.含有5 (Trim5) 的三部分图案.血管光滑肌细胞是血管光滑肌细胞.

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