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骨髓氧化酶在马凡氏病中加剧胸前大动脉动脉瘤的形成

Dennis Mehrkens^1,2, Johannes Dohr^1,2, Felix Sebastian Nettersheim^1,2

¹Faculty of Medicine and University Hospital Cologne, Clinic III for Internal Medicine, University of Cologne, Cologne, Germany.

Cardiovascular research

|December 17, 2025

概括

骨髓氧化酶 (MPO) 通过促进炎症和氧化应激,促进马芬综合征 (MFS) 大动脉扩张. 在小鼠中抑制MPO减少了大动脉动脉瘤的形成,这表明MPO是MFS的治疗标.

科学领域:

心血管生物学心血管生物学
结合组织疾病结合组织疾病
在疾病中的酶功能.

背景情况:

马凡综合征 (MFS) 是一种普遍存在的遗传性结合组织疾病,与胸前大动脉动脉瘤的过早死亡有关.
髓氧化酶 (MPO) 是一种来自白细胞的酶,对血管壁有很高的亲和力,并且研究了它在MFS相关的大动脉重塑中的作用.

研究的目的:

调查髓氧化酶 (MPO) 对马尔凡综合征 (MFS) 中大动脉重塑的贡献.
评估MPO作为MFS相关的胸前大动脉动脉瘤的潜在治疗标.

主要方法:

在MFS患者和对照组中评估了血MPO水平.
使用异质性转基因Fbn1C1041G/+ (MFS) 鼠标,MPO缺乏的MFS鼠标 (MFSxMpo-/-) 和MPO抑制剂治疗的MFS鼠标来研究胸前动脉动脉瘤的形成.
采用超声波,组织学和RNA测序来分析大动脉重塑,炎症和基因表达.

主要成果:

患有MFS的患者表现出循环MPO水平升高和大动脉MPO沉积.
在MFS小鼠中,MPO缺乏减少了大动脉弹性质碎片化和动脉瘤形成.
在MFS小鼠中MPO抑制 (AZM198) 减弱胸前动脉动脉瘤 (TAA) 发育,减少炎症,氧化应激和细胞外矩阵重塑.

结论:

髓氧化酶 (MPO) 通过驱动炎症性内皮激活,氧化应激和不利的细胞外矩阵重塑,加剧马方综合征 (MFS) 中胸前大动脉扩张.
在小鼠模型中,MPO的遗传和药理抑制都有效地减少了MFS相关的大动脉扩张.
在马尔凡综合征中,MPO代表了治疗胸前大动脉动脉瘤的有希望的治疗标.

关键词:

马方综合征 • 大动脉动脉瘤 • 炎症 • 髓氧化酶 • 内皮细胞

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