Mitochondrial complex II is a source of the reserve respiratory capacity that is regulated by metabolic sensors and promotes cell survival.
Mitochondrial complex II is a source of the reserve respiratory capacity that is regulated by metabolic sensors and promotes cell survival.
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DOI：
10.1038/cddis.2015.202
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发表时间：
2015-07-30
影响因子：
9
通讯作者：
Abdellatif M
中科院分区：
文献类型：
--
作者：
Pfleger J;He M;Abdellatif M
细胞的存活取决于其满足能量需求的能力。我们假设细胞的线粒体储备呼吸能力（RRC）是其生物能量学的关键组成部分，可以在能量需求增加期间利用，从而提高生存力。我们的目标是确定调控和促进RRC发展及其参与细胞存活的因素。结果表明，代谢传感器的激活，包括丙酮酸脱氢酶和AMP依赖性激酶，通过Sirt3依赖性机制增加心肌细胞RRC。值得注意的是，我们确定线粒体复合物II（cII）作为这些代谢传感器的目标和RRC的主要来源。此外，我们表明，RRC，通过cII，与缺氧后增强细胞存活。因此，我们第一次表明，代谢传感器通过Sirt3最大化细胞RRC通过激活cII，这增强了细胞在缺氧后的存活。
The survival of a cell depends on its ability to meet its energy requirements. We hypothesized that the mitochondrial reserve respiratory capacity (RRC) of a cell is a critical component of its bioenergetics that can be utilized during an increase in energy demand, thereby, enhancing viability. Our goal was to identify the elements that regulate and contribute to the development of RRC and its involvement in cell survival. The results show that activation of metabolic sensors, including pyruvate dehydrogenase and AMP-dependent kinase, increases cardiac myocyte RRC via a Sirt3-dependent mechanism. Notably, we identified mitochondrial complex II (cII) as a target of these metabolic sensors and the main source of RRC. Moreover, we show that RRC, via cII, correlates with enhanced cell survival after hypoxia. Thus, for the first time, we show that metabolic sensors via Sirt3 maximize the cellular RRC through activating cII, which enhances cell survival after hypoxia.