O2 sensing, mitochondria and ROS signaling: The fog is lifting.
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 in understanding this field and considers recent advances that provide new insight, helping to lift the fog from this complex topic.
['Waypa|Gregory B|GB|', 'Smith|Kimberly A|KA|', 'Schumacker|Paul T|PT|']
D000818:Animals D004195:Disease Models, Animal D006801:Humans D000860:Hypoxia D008928:Mitochondria D008954:Models, Biological D010084:Oxidation-Reduction D010100:Oxygen D017382:Reactive Oxygen Species D015398:Signal Transduction
Hypoxia electron transport chain metabolism oxidant signaling