Cellular and molecular mechanisms of O2 sensing

ER Swenson (Editor), P Bartsch (Editor), Paul T Schumacker*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapter

3 Scopus citations


Molecular oxygen is required for mitochondrial energy generation, and all eukaryotic organisms have the capacity to sense the abundance of cellular O2. When oxygen levels decrease, these sensors activate a wide range of transcriptional, translational, and posttranslational responses that protect the cell and the organism from the consequences of severe oxygen deprivation and O2-limited metabolism. A number of different mechanisms of oxygen sensing have been proposed, and it is likely that diverse cell types employ multiple means of sensing changes in molecular oxygen. However, growing evidence points to the mitochondria as an important site of O2 sensing in diverse cell types. These organelles release reactive oxygen species (ROS) signals to the cytosol where they trigger transcriptional and posttranslational adaptive responses. Although the precise molecular mechanisms underlying the increase in ROS generation under low O2 conditions are not fully understood, these signals appear to originate from complex III of the electron transport chain. The responses regulated by this mechanism include the stabilization of Hypoxia-Inducible Factor-1α and the acute vasoconstrictor response to alveolar hypoxia in the lung. Future studies of prolonged hypoxia are still needed to determine whether the responses to chronic hypoxia are also regulated by this pathway.

Original languageEnglish
Title of host publicationHigh Altitude: Human Adaptation to Hypoxia
Subtitle of host publicationHuman Adaptation to Hypoxia
PublisherSpringer New York
Number of pages22
ISBN (Electronic)9781461487722
ISBN (Print)1461487714, 9781461487715
StatePublished - Jul 1 2014

ASJC Scopus subject areas

  • General Medicine


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