Mitochondria control acute and chronic responses to hypoxia

- Mitochondrial electron transport chain function plays a key role in organismal hypoxia sensing.
- ETC Complex III ROS are necessary for acute hypoxic contraction of pulmonary smooth muscle cells.
- ETC Complex I function is essential for acute glomus cell sensing of hypoxemia in the carotid body.
- mROS are required for HIF stabilization and organismal adaptation to hypoxia.

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.