Mitochondrial complex II is a source of the reserve respiratory capacity that is regulated by metabolic sensors and promotes cell survival
作者： J Pfleger , M He , M Abdellatif
关键词: Biochemistry 、 SIRT3 、 Pyruvate dehydrogenase complex 、 Biology 、 Cell 、 Bioenergetics 、 Oxidative phosphorylation 、 Cellular respiration 、 Signal transduction 、 Mitochondrion 、 Cell biology
摘要: The survival of a cell depends on its ability to meet energy requirements. We hypothesized that the mitochondrial reserve respiratory capacity (RRC) is critical component bioenergetics can be utilized during an increase in demand, thereby, enhancing viability. Our goal was identify elements regulate and contribute development RRC involvement survival. results show activation metabolic sensors, including pyruvate dehydrogenase AMP-dependent kinase, increases cardiac myocyte via Sirt3-dependent mechanism. Notably, we identified complex II (cII) as target these sensors main source RRC. Moreover, RRC, cII, correlates with enhanced after hypoxia. Thus, for first time, Sirt3 maximize cellular through activating which enhances
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