Journal
EXPERIMENTAL CELL RESEARCH
Volume 356, Issue 2, Pages 217-222Publisher
ELSEVIER INC
DOI: 10.1016/j.yexcr.2017.03.034
Keywords
Hypoxia; Mitochondria; Reactive oxygen species; Metabolism
Categories
Funding
- NIH [R35 CA197532, PO1 AG04966502, PO1 HL071643, T32 CA9560, T32 HL076139-13]
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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.
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