Abstract
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.
Original language | English (US) |
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Pages (from-to) | 217-222 |
Number of pages | 6 |
Journal | Experimental Cell Research |
Volume | 356 |
Issue number | 2 |
DOIs | |
State | Published - Jul 15 2017 |
Funding
This work was supported by NIH (R35 CA197532, PO1 AG04966502, PO1 HL071643) to NSC, NIH (T32 CA9560) and NIH (T32 HL076139-13) to GM.
Keywords
- Hypoxia
- Metabolism
- Mitochondria
- Reactive oxygen species
ASJC Scopus subject areas
- Cell Biology