Transient exposure to hydrogen peroxide causes an increase in mitochondria-derived superoxide as a result of sustained alteration in L-type Ca2+ channel function in the absence of apoptosis in ventricular myocytes.

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作者： Helena M,Viola ^[1] ; Peter G,Arthur ; Livia C,Hool

作者单位： School of Biomedical, Biomolecular and Chemical Sciences, University of Western Australia, 35 Stirling Hwy, Crawley, WA, 6009, Australia. ^[1]

主题词动物(Animals);细胞凋亡(Apoptosis);钙(Calcium);钙通道, L型(Calcium Channels, L-Type);导电性(Electric Conductivity);胡米胺(Ethidium);豚鼠(Guinea Pigs);心室(Heart Ventricles);过氧化氢(Hydrogen Peroxide);细胞内膜(Intracellular Membranes);线粒体, 心脏(Mitochondria, Heart);心肌收缩(Myocardial Contraction);肌细胞, 心脏(Myocytes, Cardiac);氧化剂(Oxidants);膜片钳术(Patch-Clamp Techniques);超氧化物类(Superoxides);时间因素(Time Factors)

DOI 10.1161/01.RES.0000263010.19273.48

PMID 17347474

发布时间 2022-02-28

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Circulation research

2007年100卷7期

1036-44页

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Transient exposure to hydrogen peroxide causes an increase in mitochondria-derived superoxide as a result of sustained alteration in L-type Ca2+ channel function in the absence of apoptosis in ventricular myocytes.

Circulation research

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Circulation research

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Transient exposure to hydrogen peroxide causes an increase in mitochondria-derived superoxide as a result of sustained alteration in L-type Ca2+ channel function in the absence of apoptosis in ventricular myocytes.

Circulation research

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Circulation research

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