Extracellular superoxide dismutase protects the heart against oxidative stress and hypertrophy after myocardial infarction
Extracellular superoxide dismutase protects the heart against oxidative stress and hypertrophy after myocardial infarction
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DOI：
10.1016/j.freeradbiomed.2007.12.007
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发表时间：
2008-04-01
影响因子：
7.4
通讯作者：
Chen, Yingjie
中科院分区：
文献类型：
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作者：
van Deel, Eiza D.;Lu, Zhongbing;Chen, Yingjie
细胞外超氧化物歧化酶 (EC-SOD) 仅占心脏总 SOD 活性的一小部分，但其重要位置是清除细胞外室中的自由基。 EC-SOD 表达在心肌梗死 (MI) 诱导的心力衰竭中降低，但 EC-SOD 是否可以消除氧化应激或改变 MI 诱导的心室重构尚未研究。因此，在对照条件下以及永久冠状动脉结扎后 4 周和 8 周时，在 EC-SOD KO 和野生型小鼠中研究了 EC-SOD 基因缺陷 (EC-SOD KO) 对左心室 (LV) 氧化应激、肥厚和纤维化的影响。 EC-SOD KO 对正常心脏的左心室功能没有可检测到的影响，但引起左心室纤维化的小幅但显着的增加。 MI 后 8 周，EC-SOD KO 小鼠的左心室肥大程度显着增加（KO 小鼠的左心室质量增加了 1.64 倍，而野生型小鼠的左心室质量增加了 1.35 倍；p
Extracellular superoxide dismutase (EC-SOD) contributes only a small fraction to total SOD activity in the heart but is strategically located to scavenge free radicals in the extracellular compartment. EC-SOD expression is decreased in myocardial-infarction (MI)-induced heart failure, but whether EC-SOD can abrogate oxidative stress or modify MI-induced ventricular remodeling has not been previously studied. Consequently, the effects of EC-SOD gene deficiency (EC-SOD KO) on left ventricular (LV) oxidative stress, hypertrophy, and fibrosis were studied in EC-SOD KO and wild-type mice under control conditions, and at 4 and 8 weeks after permanent coronary artery ligation. EC-SOD KO had no detectable effect on LV function in normal hearts but caused small but significant increases of LV fibrosis. At 8 weeks after MI, EC-SOD KO mice developed significantly more LV hypertrophy (LV mass increased 1.64-fold in KO mice compared to 1.35-fold in wild-type mice; p