Some Aspects of the Mitochondrial KATP Channel Functioning under Hypoxia

Oxygen deficit is known to produce profound alterations to mitochondrial functions and metabolism. Primarily, it concerns the complexes of the respiratory chain, the functions of antioxidant and pro-oxidant enzyme systems in the cell and mitochondria, pathways of ATP synthesis, ROS production and signaling. But one common feature of the metabolic alterations in mitochondria under hypoxia is the activation of mitochondrial potassium transport. The system of mitochondrial potassium transport is represented by several types of potassium channels and K+/H+ exchanger, which acting coordinately constitute potassium cycle. Potassium transport is an all-round modulator of mitochondrial functions: oxygen consumption, Ca2+ transport, ATP synthesis, ROS production and matrix volume. But what are the functions of potassium transport and which are the benefits of the activation of potassium channels under hypoxia? The purpose of this mini-review is an attempt to find answers to these questions based on the published data and the results of the author’s research.