title: O2 sensing, mitochondria and ROS signaling: The fog is lifting.
abstract: 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.
authors.affiliation: Department of Pediatrics, Division of Neonatology, Northwestern University, Feinberg School of Medicine, Chicago, IL, USA.
authors.forename: Gregory B
authors.initials: GB
authors.lastname: Waypa
authors.affiliation: Department of Pediatrics, Division of Neonatology, Northwestern University, Feinberg School of Medicine, Chicago, IL, USA.
authors.forename: Kimberly A
authors.initials: KA
authors.lastname: Smith
authors.affiliation: Department of Pediatrics, Division of Neonatology, Northwestern University, Feinberg School of Medicine, Chicago, IL, USA. Electronic address: p-schumacker@northwestern.edu.
authors.forename: Paul T
authors.initials: PT
authors.lastname: Schumacker
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D000860:Hypoxia / Q000378:metabolism; D008928:Mitochondria / Q000378:metabolism*; D008954:Models, Biological; D010084:Oxidation-Reduction; D010100:Oxygen / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction
chemical_list: D017382:Reactive Oxygen Species; D010100:Oxygen
keywords: Hypoxia; electron transport chain; metabolism; oxidant signaling