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There are numerous mechanisms by which mammals respond to hypoxia. These include acute changes in pulmonary arterial tone due to smooth muscle cell contraction, acute increases in respiration triggered by the carotid body chemosensory cells, and chronic changes such as induction of red blood cell proliferation and angiogenesis by hypoxia inducible factor targets erythropoietin and vascular endothelial growth factor, respectively. Mitochondria account for the majority of oxygen consumption in the cell and have recently been appreciated to serve as signaling organelles required for the initiation or propagation of numerous homeostatic mechanisms. Mitochondria can influence cell signaling by production of reactive oxygen species and metabolites. Here we review recent evidence that mitochondrial signals can imitate acute and chronic hypoxia responses. [ABSTRACT FROM AUTHOR]

Looks at a study which investigated the hypothesis that mitochondria which increased the generation of reactive oxygen species (ROS) during hypoxia, acted as O2 sensors. In-depth look at mammalian cells; Details on the transcriptional activation of erythropoietin and the vascular endothelial growth factor; Methodology used to conduct the study; Results of the study.