Mitochondrial Channels as Potential Targets for Pharmacological Strategies in Brain Ischemia

Ischemic stroke is a major cause of death and disability urgently requiring novel therapeutic approaches. Deprivation of oxygen and respiratory substrate during an ischemic episode has its most immediate impact on mitochondria, the body’s primary oxygen consumers. Mitochondrial function is in turn critically dependent on a range of carriers and channels, most of which remain inadequately understood at the genetic and molecular level. As mitochondrial channels are involved in energy production, calcium handling, generation of reactive oxygen species (ROS) and cell-death related signaling, it is evident that increased understanding of these processes and their regulation will help the search for novel rational approaches to therapy.