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腹腔大动脉动脉瘤的早期进展通过通过ALDH2-LIN28B-ELK3信号传输来改善内皮屏障功能来减缓

Kehui Yang^1,2,3, Sumei Cui^1,2,3, Jingwen Wang^1,2,3

¹Department of Emergency Medicine, Chest Pain Center, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|October 12, 2023

概括

干扰的内皮屏障功能有助于腹腔大动脉动脉瘤 (AAA). 内皮细胞 (ECs) 中的脱酶2 (ALDH2) 保持了屏障完整性,提供了潜在的早期AAA治疗策略.

科学领域:

血管生物学血管生物学
动脉样硬化研究动脉样硬化研究
内皮细胞生物学内皮细胞生物学

背景情况:

内皮屏障功能障碍与腹腔大动脉动脉瘤 (AAA) 病变发生有关.
在AAA中,内皮屏障功能的上游调节者在很大程度上仍然没有表征.
ангиотензин II (Ang II) 输注是研究AAA发育的一个模型.

研究的目的:

调查内皮屏障功能在Ang II诱导的AAA中的作用.
在AAA早期确定内皮屏障完整性的上游调节者.
在AAA中探索向内皮屏障功能的治疗潜力.

主要方法:

单细胞RNA测序 (scRNA-seq) 的AngII注入的小鼠大动脉.
人类大动脉剖析组织的mRNA测序.
甲基脱酶2 (ALDH2) 在内皮细胞 (ECs) 中的敲除/敲除.
评估内皮壁标记,完整性和大动脉扩张的评估.

主要成果:

在AAA进展的早期观察到受损的内皮焦点连接和下调的屏障基因.
在人类AAA组织中,ALDH2被上调,并调节了EC屏障功能.
降低EC中的ALDH2恢复了屏障完整性,并抑制了早期Ang II诱导的AAA.
ALDH2通过LIN28B直接调节ELK3的表达,影响内皮屏障功能.

结论:

内皮屏障功能障碍是AAA发展的早期事件.
在早期AAA期间,ALDH2在维持内皮屏障完整性方面发挥着保护作用.
在EC中准ALDH2为早期AAA管理提供了潜在的治疗策略.

关键词:

在ELK3中,ELK3是ELK3.腹部大动脉动脉瘤腹部大动脉动脉瘤阿尔德海德脱酶2的使用它们是内皮细胞的内皮细胞.启动启动启动

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