O2 sensing, mitochondria and ROS signaling: The fog is lifting.
O2 sensing, mitochondria and ROS signaling: The fog is lifting.
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DOI：
10.1016/j.mam.2016.01.002
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发表时间：
2016-02
影响因子：
10.6
通讯作者：
Schumacker PT
中科院分区：
文献类型：
--
作者：
Waypa GB;Smith KA;Schumacker PT
线粒体负责细胞中的大部分氧消耗，因此代表了细胞氧传感的概念上有吸引力的位点。在过去的40年里，已经提出了许多解释线粒体如何参与氧传感的机制。然而，关于线粒体如何调节缺氧的转录和翻译后反应还没有达成共识。然而，越来越多的数据继续暗示来自电子传递链（ETC）的活性氧（ROS）信号增加在触发不同细胞类型对缺氧的反应中的作用。本文回顾了我们对这一领域的理解，并考虑了最近的进展，提供了新的见解，有助于解除这一复杂主题的迷雾。
Mitochondria are responsible for the majority of oxygen consumption in cells, and thus represent a conceptually appealing site for cellular oxygen sensing. Over the past 40 years a number of mechanisms to explain how mitochondria participate in oxygen sensing have been proposed. However, no consensus has been reached regarding how mitochondria could regulate transcriptional and post-translational responses to hypoxia. Nevertheless, a growing body of data continues to implicate a role for increased reactive oxygen species (ROS) signals from the electron transport chain (ETC) in triggering responses to hypoxia in diverse cell types. The present article reviews our progress understanding this field and considers recent advances that provide new insight, helping to lift the fog from this complex topic.