Mitochondrial K+ Transport: Modulation and Functional Consequences

The existence of a K+ cycle in mitochondria has been predicted since the development of the chemiosmotic theory and has been shown to be crucial for several cellular phenomena, including regulation of mitochondrial volume and redox state. One of the pathways known to participate in K+ cycling is the ATP-sensitive K+ channel, MitoK(ATP). This channel was vastly studied for promoting protection against ischemia reperfusion when pharmacologically activated, although its molecular identity remained unknown for decades. The recent molecular characterization of MitoK(ATP) has opened new possibilities for modulation of this channel as a mechanism to control cellular processes. Here, we discuss different strategies to control MitoK(ATP) activity and consider how these could be used as tools to regulate metabolism and cellular events.

Automated summary

The existence of a K+ cycle in mitochondria is crucial for regulating cellular processes, with the MitoK(ATP) channel being studied for its protective effects against ischemia reperfusion injury. The recent molecular characterization of MitoK(ATP) has opened up new possibilities for modulating this channel for regulating cellular events.