Overexpressing superoxide dismutase 2 induces a supernormal cardiac function by enhancing redox-dependent mitochondrial function and metabolic dilation
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- 作者：Patrick T. Kang ; Chwen-Lih Chen ; Vahagn Ohanyan ; Daniel J. Luther ; J. Gary Meszaros ; William M. Chilian ; Yeong-Renn Chen ; ychen1@neomed.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：SOD2 ; manganese-containing superoxide dismutase ; SOD2-tg ; transgenic mice with cardiac-specific SOD2 overexpression ; RPP ; rate pressure product ; MBF ; myocardial blood flow ; HR ; heart rate ; MAP ; mean arterial pressure ; EDHF ; endothelium-derived hyperpolarizing factor ; GPx2 ; mitochondrial glutathione peroxidase ; NQR ; NADH ubiquinone reductase ; or mitochondrial complex I ; SCR ; succinate cytochrome c reductase ; O2&minus ; ; superoxide anion radical ; ROS ; reactive oxygen species ; ETC ; electron tr
- 刊名：Journal of Molecular and Cellular Cardiology
- 出版年：2015
- 出版时间：November 2015
- 年：2015
- 卷：88
- 期：Complete
- 页码：14-28
- 全文大小：2037 K
文摘
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Gene delivery of SOD2 is widely applied to pre-clinical studies.
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Cardiac SOD2 overexpression enhances mitochondrial ATP/O ratio and reductive status.
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Cardiac SOD2 overexpression boosts metabolic vasodilation and myocardial perfusion.
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SOD2 overexpression in myocytes prevents L-NAME induced myocardial injury.
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SOD2 overexpression in myocytes improves overall cardiac function.