Mitochondria-specific transgenic overexpression of phospholipid hydroperoxide glutathione peroxidase (GPx4) attenuates ischemia/reperfusion-associated cardiac dysfunction
Mitochondria-specific transgenic overexpression of phospholipid hydroperoxide glutathione peroxidase (GPx4) attenuates ischemia/reperfusion-associated cardiac dysfunction
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DOI：
10.1016/j.freeradbiomed.2008.06.021
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发表时间：
2008-09-15
影响因子：
7.4
通讯作者：
Hollander, John M.
中科院分区：
文献类型：
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作者：
Dabkowski, Erinne R.;Williamson, Courtney L.;Hollander, John M.
缺血/再灌注 (I/R) 损伤会引起线粒体损伤。抗氧化剂可防止缺血再灌注引起的线粒体损伤。本研究的目的是确定线粒体特异性 GPx4 (PHGPx) 过度表达对 I/R 后心脏功能的影响。创建了转基因小鼠，其中 PHGPx 仅在线粒体 (mPHGPx) 中过表达。 MPHGPx 和同窝对照心脏经历整体无血流缺血（20 分钟），然后进行回流再灌注（30、60 和 90 分钟）。 I/R 后，与对照组相比，mPHGPx 心脏具有明显更好的收缩率、发展压力和收缩压峰值（P
Ischemia/reperfusion (I/R) injury elicits damage to mitochondria. Antioxidants provide protection from I/R-induced mitochondrial damage. The goal of this study was to determine the impact of mitochondria-specific overexpression of GPx4 (PHGPx) on cardiac function following I/R. Transgenic mice were created in which PHGPx was overexpressed solely in the mitochondrion (mPHGPx). MPHGPx and littermate control hearts were subjected to global no-flow ischemia (20 min) followed by reflow reperfusion (30, 60, and 90 min). Following I/R, mPHGPx hearts possessed significantly better rates of contraction, developed pressures, and peak-systolic pressures as compared to controls (P