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抑制NOX2通过通过MertK/PI3K/AKT通路增强巨细胞效应,稳定脆弱的斑块

Yue Wang¹, Xin-Yan Liu¹, Yue Wang¹

¹Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.

|June 24, 2023

概括

抑制NADPH氧化酶2 (NOX2) 通过降低ROS和通过MertK/PI3K/AKT通路增强巨细胞分裂,防止易受损伤的斑块发育. 这项研究揭示了一种新的NOX2-ROS-MerTK轴在斑块病变发生过程中.

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.
动脉样硬化研究动脉样硬化研究

背景情况:

NADPH氧化酶2 (NOX2) 产生反应性氧物种 (ROS),对于动脉样硬化发展至关重要.
在已建立的脆弱斑块中NOX2抑制的确切作用仍然在很大程度上是未知的.

研究的目的:

阐明NOX2抑制影响脆弱斑块进展的潜在机制.
为了研究NOX2-ROS-MerTK信号轴在巨细胞增生和斑块稳定性.

主要方法:

使用手术绑定,动脉收缩和高脂肪饮食,建立了一个易受伤害的鼻斑块小鼠模型 (ApoE-/-).
小鼠用NOX2抑制剂GSK2795039治疗了8周,通过微超声波评估了斑块的进展.
在体内和体外分析了巨细胞和相关的信号通路 (MertK/PI3K/AKT).

主要成果:

治疗GSK2795039显著抑制了易受损的斑块形成,改善了斑块稳定性标记 (增加原脂比,纤维帽厚度;减少核和斑块内出血).
抑制NOX2导致氧化应激 (4-HNE) 降低,损伤性亡减少,并增强了巨细胞增生.
在巨细胞中,NOX2抑制通过激活MertK/PI3K/AKT通路促进了效细胞分裂.

结论:

NOX2在脆弱的动脉样硬化斑块的发病过程中发挥着重要作用.
抑制NOX2为稳定易受损伤的斑块提供了一个潜在的治疗策略.
确定了一种新的NOX2-ROS-MerTK信号通路,该通路调节了斑块发育中的巨细胞细胞分裂.

关键词:

动脉样硬化是一种动脉样硬化.有效的细胞分裂.梅尔特克是因为氧二氧化 (NOX2) 是一种易受伤害的斑块是容易受伤害的

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