Mitochondria-targeted antioxidant (MitoQ) ameliorates age-related arterial endothelial dysfunction in mice
Mitochondria-targeted antioxidant (MitoQ) ameliorates age-related arterial endothelial dysfunction in mice
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DOI：
10.1113/jphysiol.2013.268680
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发表时间：
2014-06-15
影响因子：
5.5
通讯作者：
Seals, Douglas R.
中科院分区：
文献类型：
--
作者：
Gioscia-Ryan, Rachel A.;LaRocca, Thomas J.;Seals, Douglas R.
心血管疾病（CVD）发展的关键前因--血管相关的动脉内皮功能障碍主要是由氧化应激导致的一氧化氮（NO）生物利用度降低引起的。当线粒体失调时，线粒体是血管氧化应激的主要来源和靶点。线粒体失调与原发性衰老有关，但其在年龄相关的内皮功能障碍中的作用尚不清楚。我们的目的是确定一种靶向抗氧化剂MitoQ在改善老年小鼠血管内皮功能障碍方面的疗效。与年轻小鼠（约8个月）相比，老年小鼠（约27个月）的离体颈动脉内皮依赖性舒张（EDD）对增加剂量的乙酰胆碱的损害约为30%，这是由于NO生物利用度降低（P
Age-related arterial endothelial dysfunction, a key antecedent of the development of cardiovascular disease (CVD), is largely caused by a reduction in nitric oxide (NO) bioavailability as a consequence of oxidative stress. Mitochondria are a major source and target of vascular oxidative stress when dysregulated. Mitochondrial dysregulation is associated with primary ageing, but its role in age-related endothelial dysfunction is unknown. Our aim was to determine the efficacy of a mitochondria-targeted antioxidant, MitoQ, in ameliorating vascular endothelial dysfunction in old mice. Ex vivo carotid artery endothelium-dependent dilation (EDD) to increasing doses of acetylcholine was impaired by approximate to 30% in old (approximate to 27months) compared with young (approximate to 8months) mice as a result of reduced NO bioavailability (P