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

W1518677196 · 수집 2026-10-04 18:12:13

T10409 Fuel Cells and Related Materials

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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.

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