通过增强NF-κBp65/CCL2信号通路,RhoA/ROCK1会加剧横向大动脉收缩引起的心房动
Mingzhi Wan1, Yao Li2, Nana Qin3
1State Key Laboratory of Frigid Zone Cardiovascular Disease, Department of Cardiovascular Surgery, General Hospital of Northern Theater Command, 83 Wenhua Road, Shenyang, Liaoning 110016, China; China Medical University, Shenyang, Liaoning 110122, China.
Cellular signalling
|November 29, 2025
概括
拉斯同类基因家族成员A (RhoA) /rho-kinase 1 (ROCK1) 途径通过促进炎症恶化心房动. 用法苏迪尔抑制RhoA/ROCK1为心房动提供了一个潜在的治疗策略.
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.
- 药理学 药理学是指药理学的学科.
背景情况:
- 心房动 (AF) 涉及心房重塑,但治疗方法有限.
- 该RhoA/ROCK1通路调节细胞骨动力学和炎症,但其在AF中的作用尚不清楚.
研究的目的:
- 研究RhoA/ROCK1信号通路在心房炎症和AF病变发生过程中的作用.
- 探索RhoA/ROCK1抑制在AF中的治疗潜力.
主要方法:
- 在心房重塑和AF的背景下,研究了RhoA/ROCK1信号的激活.
- 使用法苏迪尔来抑制RhoA/ROCK1,并评估其对心房纤维化,炎症和AF诱导性的影响.
- 研究了核因子kappa-B p65 (NF-κBp65) /化学因子C-C-Motif连接物2 (CCL2) 途径的参与.
主要成果:
- 罗亚/ROCK1激活加剧了心房炎症和重塑,增加了AF易感性.
- 法苏迪尔治疗减轻了心房纤维化,炎症和AF诱导性.
- 抑制RhoA/ROCK1可以抑制NF-κBp65/CCL2信号通路.
- 恢复NF-κBp65表达可以否定fasudil的保护作用.
结论:
- 罗亚/ROCK1通路是压力过载引起的AF的关键调解者.
- 罗亚/ROCK1-NF-κB/CCL2轴是AF治疗的一个有前途的治疗标.
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