Ectopic overexpression of Kir6.1 in the mouse heart impacts on the life expectancy.

ABSTRACT: We recently reported the reduced ATP-sensitive potassium (K_ATP) channel activities in the transgenic mouse heart overexpressing the vascular type K_ATP channel pore-forming subunit (Kir6.1). Although dysfunction of cardiac K_ATP channel has been nominated as a cause of cardiomyopathy in human, these transgenic mice looked normal as wild-type (WT) during the experiment period (~20 weeks). Extended observation period revealed unexpected deaths beginning from 30 weeks and about 50% of the transgenic mice died by 55 weeks. Surface ECG recordings from the transgenic mice at rest demonstrated the normal sinus rhythm and the regular ECG complex as well as the control WT mice except for prolonged QT interval. However, the stress ECG test with noradrenaline revealed a

SUBMITTER: Watanabe Y 

PROVIDER: S-EPMC6078942 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature