Nicotine induces vasa vasorum stenosis in the aortic wall

被引:1
|
作者
Kugo, Hirona [1 ]
Moriyama, Tatsuya [1 ,2 ]
Zaima, Nobuhiro [1 ,2 ]
机构
[1] Kindai Univ, Grad Sch Agr, Dept Appl Biol Chem, 204-3327 Nakamachi, Nara 6318505, Japan
[2] Kindai Univ, Agr Technol & Innovat Res Inst, Nara, Japan
基金
日本学术振兴会;
关键词
Abdominal aortic aneurysm; nicotine; hypoperfusion; hypoxia; vasa vasorum; ELASTIN FIBERS; INTRALUMINAL THROMBUS; DEGRADATION; ANEURYSM; HYPOXIA; ACTIVATION; COLLAGEN; SMOKING; MMP-2;
D O I
10.1080/10520295.2024.2352724
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Abdominal aortic aneurysm (AAA) is a vascular disease that involves aortic wall dilation. Cigarette smoking is an established risk factor and rupture, and nicotine may be a major contributor to the onset of AAA. In humans the condition is associated with stenosis of the vasa vasorum (VV), which may be caused by nicotine. In this study, we evaluated the effects of nicotine on VV pathology. After 4 weeks of nicotine administration to rats using an osmotic pump, the VV patency rate in the nicotine administration group was significantly lower than that in the control group. The levels of Ki-67, a cell proliferation marker, were significantly increased in the regions containing VV in the nicotine group, as were hypoxia inducible factor-alpha levels. Collagen levels around VV were significantly lower in the nicotine group than in the controls. Our data suggest that nicotine can cause VV stenosis by inducing abnormal proliferation of smooth muscle cells in the VV. The increased risk of AAA development due to cigarette smoking may be partially explained by nicotine-induced VV denaturation and collagen fiber degradation.
引用
收藏
页码:197 / 203
页数:7
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