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Mitochondrial reactive oxygen species regulate hypoxic signaling

机译:线粒体活性氧调节缺氧信号

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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.
机译:生理性缺氧导致许多反应,包括通气增加,肺动脉收缩和促进糖酵解,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耗者,因此多年来一直被认为是细胞氧气感测的场所。现在已知许多对缺氧的细胞反应是由线粒体复合物III上活性氧的产生介导的。虽然尚不清楚缺氧期间细胞内氧化剂浓度增加的机制,但维持细胞氧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在细胞氧信号中的作用的当前理解的简要概述。

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