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特定于VSMC的TRPC1缺失减轻了血管激素II诱导的高血压和心血管重塑

Xin Wen¹, Yuefeng Peng¹, Wenqing Yang¹

¹Wuxi School of Medicine, Jiangnan University, Jiangsu Province, 1800 Lihu Rd, Wuxi, 214122, China.

Journal of molecular medicine (Berlin, Germany)

|January 1, 2025

概括

血管光滑肌细胞中的暂时受体潜在正规1 (TRPC1) 通道通过促进细胞增殖和迁移,驱动高血压和心血管损伤. 抑制TRPC1或EZH2减轻了这些影响,表明了治疗潜力.

科学领域:

心血管生物学心血管生物学
分子医学是分子医学.
高血压研究高血压研究

背景情况:

暂时受体潜在的正规 1 (TRPC1) 通道是血管系中发现的 Ca2+ 透性离子通道.
特别是来自血管光滑肌细胞 (VSMC) 的TRPC1在高血压和心脏重塑中的作用尚未完全理解.

研究的目的:

研究VSMC衍生的TRPC1在血管素II (AngII) 诱导的高血压和心血管改造中的病理生理作用.
阐明连接AngII,TRPC1和高血压心血管损伤的分子机制.

主要方法:

在AngII治疗的VSMC和小鼠大心脏中评估TRPC1表达.
利用特定于VSMC的TRPC1缺乏的小鼠来评估AngII诱导的影响.
调查了增强器的作用胃肠同源2 (EZH2) 和MEK-ERK途径在调解TRPC1功能.
服用EZH2抑制剂以评估治疗疗效.

主要成果:

在AngII治疗的VSMCs和aortas中观察到TRPC1表达的增加.
特定于VSMC的TRPC1缺陷减轻了AngII诱导的血管收缩,高血压,血管改造和心脏缩.
AngII激活了EZH2,导致TRPC1表达增加,流入和MEK-ERK激活,促进VSMC的增殖和迁移.
抑制EZH2降低了VSMC的扩散/迁移,并缓解了高血压和血管收缩.

结论:

EZH2-TRPC1-MEK/ERK通路在AngII诱导的高血压和心血管损伤中发挥着关键作用.
在VSMC中的TRPC1对高血压血管和心脏重塑有显著的贡献.
针对TRPC1或EZH2是一个潜在的高血压治疗策略.

关键词:

ангиотензин II 的使用.在 EZH2 中使用.在高血压的高血压.TRPC1 是一个人.血管光滑肌细胞是血管光滑肌细胞

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