在先天性大动脉形缺陷中,大动脉扩张的潜在机制
D Bonderman1, E Gharehbaghi-Schnell, G Wollenek
1departments of Cardiology and Cardiothoracic Surgery (G.W.), University of Vienna; and the Ludwig Boltzmann Institute for Cardiovascular Research, Vienna, Austria.
Circulation
|April 27, 1999
概括
大动脉组织中过早的细胞死亡与大动脉缺陷有关. 这项研究揭示了大动脉形异常患者的亡增加,这表明大动脉疾病的遗传基础.
科学领域:
- 心血管病理学心血管病理学
- 细胞生物学 细胞生物学
- 遗传学 是一个遗传学.
背景情况:
- 大动脉疾病,包括扩张,动脉瘤和剖析,经常与先天性大动脉膜形一起发生.
- 受影响的大动脉的组织学发现经常显示埃尔德海姆囊性中间性亡 (CMN),其特征是光滑肌肉细胞损失和组织退化.
研究的目的:
- 为了研究细胞亡 (编程细胞死亡) 是否有助于CMN和光滑肌肉细胞在大动脉中间层的损失.
- 为了将亡率与大动脉形态以及大动脉扩张的存在相关联.
主要方法:
- 对32名接受心胸外科手术的患者的上升性大动脉壁样本的分析.
- 组织化学染色和终端脱氧核乙烯转移酶介导的脱氧氨酸三酸盐末标记 (TUNEL) 以检测亡.
- 根据心声学,将患者分为四组:双或三大动脉,有或没有大动脉扩张.
主要成果:
- 在有大动脉扩张的患者的中间层观察到大规模的焦点亡,无论门类型 (双或三).
- 与非扩张的大动脉相比,在扩张的大动脉中发现了中部光滑肌肉细胞亡的显著更高的比率.
- 双膜和大动脉扩张的患者比三膜和扩张的患者年轻.
结论:
- 中部光滑肌细胞的过早亡可能是驱动大动脉疾病的遗传机制的关键组成部分,在患有大动脉异常的人中.
- 亡可能是与各种主动脉异常相关的主动脉疾病病变的常见途径.
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