Overexpression of farnesyl pyrophosphate synthase increases myocardial ischemia/reperfusion injury in mice

被引：3

作者：

Dai, Dongpu ^{[1
]}

Sun, Xiaotong ^{[1
]}

Ding, Jie ^{[1
]}

Chen, Yuxiao ^{[1
]}

Hu, Shenjiang ^{[1
]}

机构：

[1] Zhejiang Univ, Coll Med, Affiliated Hosp 1, Inst Cardiol, 79 Qing Chun Rd, Hangzhou 310003, Zhejiang, Peoples R China

来源：

GENE | 2018年 / 672卷

关键词：

Reactive oxygen species; Rac1; Langendorff; REPERFUSION INJURY; FREE-RADICALS; IN-VIVO; RAC1; INHIBITION; PROTECTION; OXIDASE; LIVER; HEART; MECHANISMS;

D O I：

10.1016/j.gene.2018.05.116

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

Famesyl pyrophosphate synthase (FPPS) is a vital enzyme in the mevalonate pathway. Our previous study has indicated that overexpression of FPPS increases hypoxia/reoxygenation (HR) injury in Heart-derived H9c2 Cells. Hence, we designed this experiment to further investigate the effect of FPPS on myocardial ischemia/reperfusion (MIR) injury using a transgenic (Tg) model, and explore the relevant mechanisms. The results showed that when mouse hearts were subjected to ex vivo I/R, Tg mice have a higher CK and LDH, a larger myocardial infarct size and lower heart function recovery. These phenomena are associated with the increased Rac1 activity and ROS generation. These findings point to that FPPS might be a potential target in preventing MIR in vivo.

引用

页码：72 / 78

页数：7

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