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• W1518677196 abstract "Mitochondrial ATP-sensitive potassium channel (mito<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M2><mml:mrow><mml:msub><mml:mrow><mml:mtext>K</mml:mtext></mml:mrow><mml:mrow><mml:mtext>ATP</mml:mtext></mml:mrow></mml:msub></mml:mrow></mml:math>) is a common end effector of many protective stimuli in myocardial ischemia-reperfusion injury (MIRI). However, the specific molecular mechanism underlying its myocardial protective effect is not well elucidated. We characterized an anoxia/reoxygenation (A/R) model using freshly isolated adult rat cardiomyocytes. Mito<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M3><mml:mrow><mml:msub><mml:mrow><mml:mtext>K</mml:mtext></mml:mrow><mml:mrow><mml:mtext>ATP</mml:mtext></mml:mrow></mml:msub></mml:mrow></mml:math>status was interfered with its specific opener diazoxide (DZ) or blocker 5-hydroxydecanote (5-HD). Digital gene expression (DGE) and bioinformatic analysis were deployed. Three energy metabolism related genes ( MT-ND6, Idh2, and Acadl ) were upregulated when mito<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M4><mml:mrow><mml:msub><mml:mrow><mml:mtext>K</mml:mtext></mml:mrow><mml:mrow><mml:mtext>ATP</mml:mtext></mml:mrow></mml:msub></mml:mrow></mml:math>opened. In addition, as many as 20 differentially expressed genes (DEGs) were significantly enriched in five energy homeostasis correlated pathways (PPAR, TCA cycle, fatty acid metabolism, and peroxisome). These findings indicated that mito<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M5><mml:mrow><mml:msub><mml:mrow><mml:mtext>K</mml:mtext></mml:mrow><mml:mrow><mml:mtext>ATP</mml:mtext></mml:mrow></mml:msub></mml:mrow></mml:math>opening in MIRI resulted in energy mobilization, which was confirmed by measuring ATP content in cardiomyocytes. These causal outcomes could be a molecular mechanism of myocardial protection of mito<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M6><mml:mrow><mml:msub><mml:mrow><mml:mtext>K</mml:mtext></mml:mrow><mml:mrow><mml:mtext>ATP</mml:mtext></mml:mrow></mml:msub></mml:mrow></mml:math>and suggested that the mito<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M7><mml:mrow><mml:msub><mml:mrow><mml:mtext>K</mml:mtext></mml:mrow><mml:mrow><mml:mtext>ATP</mml:mtext></mml:mrow></mml:msub></mml:mrow></mml:math>opening plays a physiologic role in triggering cardiomyocytes’ energy homeostasis during MIRI. Strategies of modulating energy expenditure during myocardial ischemia-reperfusion may be promising approaches to reduce MIRI." @default.
• W1518677196 created "2016-06-24" @default.
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• W1518677196 date "2015-01-01" @default.
• W1518677196 modified "2023-10-02" @default.
• W1518677196 title "Genome-Wide Expression Profiling of Anoxia/Reoxygenation in Rat Cardiomyocytes Uncovers the Role of Mito<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M1><mml:mrow><mml:msub><mml:mrow><mml:mtext mathvariant=bold>K</mml:mtext></mml:mrow><mml:mrow><mml:mtext mathvariant=bold>ATP</mml:mtext></mml:mrow></mml:msub></mml:mrow></mml:math>in Energy Homeostasis" @default.
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• W1518677196 doi "https://doi.org/10.1155/2015/756576" @default.
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