Involvement of mitochondrial permeability transition pore (mPTP) in cardiac arrhythmias: Evidence from cyclophilin D knockout mice
Involvement of mitochondrial permeability transition pore (mPTP) in cardiac arrhythmias: Evidence from cyclophilin D knockout mice
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DOI：
10.1016/j.ceca.2016.09.001
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发表时间：
2016-12-01
期刊：
影响因子：
4
通讯作者：
Xie, Lai-Hua
中科院分区：
文献类型：
--
作者：
Gordan, Richard;Fefelova, Nadezhda;Xie, Lai-Hua
在本研究中，我们使用缺乏亲环蛋白D （CypD KO）的遗传小鼠模型来评估线粒体通透性过渡孔（mPTP）抑制对单细胞水平Ca2+波和Ca2+交替以及全心制剂中心律失常的心脏保护作用。原细胞羰基氰化对-（三氟甲氧基）苯腙（FCCP）在WT和CypD KO小鼠心肌细胞中引起线粒体膜电位去极化的程度相同，但CypD KO小鼠心肌细胞的mPTP开放程度明显低于WT小鼠(p
In the present study, we have used a genetic mouse model that lacks cyclophilin D (CypD KO) to assess the cardioprotective effect of mitochondrial permeability transition pore (mPTP) inhibition on Ca2+ waves and Ca2+ alternans at the single cell level, and cardiac arrhythmias in whole-heart preparations. The protonophore carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP) caused mitochondrial membrane potential depolarization to the same extent in cardiomyocytes from both WT and CypD KO mice, however, cardiomyocytes from CypD KO mice exhibited significantly less mPTP opening than cardiomyocytes from WT mice (p