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线粒体对氧感受的调节。

Mitochondrial regulation of oxygen sensing.

机构信息

Division of Pulmonary and Critical Care Medicine, Department of Medicine, Northwestern University, Chicago, IL, 606011, USA.

出版信息

Adv Exp Med Biol. 2010;661:339-54. doi: 10.1007/978-1-60761-500-2_22.

Abstract

Hypoxia promotes physiological processes such as energy metabolism, angiogenesis, cell proliferation, and cell viability through the transcription factor Hypoxia Inducible Factor (HIF). Hypoxia also diminishes the activity of ATP consuming processes to promote cell survival. The mechanism(s) by which hypoxia activates HIF and diminishes ATP demand are a subject of intensive research. Here we outline the model in which mitochondrial complex III regulate the activity of HIF and diminish ATP utilization processes through the increased production of ROS during hypoxia.

摘要

缺氧通过转录因子缺氧诱导因子 (HIF) 促进能量代谢、血管生成、细胞增殖和细胞活力等生理过程。缺氧还会降低消耗 ATP 的过程的活性,以促进细胞存活。缺氧激活 HIF 和降低 ATP 需求的机制是一个密集研究的课题。在这里,我们概述了一种模型,即在缺氧期间通过增加 ROS 的产生,线粒体复合物 III 调节 HIF 的活性并降低 ATP 利用过程。

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