Department of Medicine, Division of Pulmonary and Critical Care Medicine, Northwestern University Medical School, Chicago, IL 60611, USA.
Curr Opin Cell Biol. 2009 Dec;21(6):894-9. doi: 10.1016/j.ceb.2009.08.005. Epub 2009 Sep 24.
Physiological hypoxia results in a host of responses that include increased ventilation, constriction of the pulmonary artery, and a cellular transcriptional program that promotes glycolysis, angiogenesis, and erythropoiesis. Mitochondria are the primary consumers of cellular oxygen and have thus been speculated for years to be the site of cellular oxygen sensing. Many of the cellular responses to hypoxia are now known to be mediated by the production of reactive oxygen species at mitochondrial complex III. While the mechanism by which cytosolic oxidant concentration is increased during hypoxia is unknown, the importance of the maintenance of cellular oxygen supply requires further investigation into the role of ROS as hypoxia signaling molecules. The following is a brief overview of the current understanding of the role of mitochondrial-produced ROS in cellular oxygen signaling.
生理性缺氧会引起一系列反应，包括增加通气、肺动脉收缩以及促进糖酵解、血管生成和红细胞生成的细胞转录程序。线粒体是细胞氧气的主要消费者，因此多年来一直推测线粒体是细胞氧气感应的部位。现在已知许多细胞对缺氧的反应是通过线粒体复合物 III 产生的活性氧物质来介导的。虽然在缺氧期间细胞质氧化剂浓度增加的机制尚不清楚，但维持细胞氧气供应的重要性需要进一步研究 ROS 作为缺氧信号分子的作用。以下是对线粒体产生的 ROS 在细胞氧气信号中的作用的当前理解的简要概述。
