Mitochondrial uncoupling as a potential therapeutic target in acute central nervous system injury
Article first published online: 17 SEP 2004
Journal of Neurochemistry
Volume 91, Issue 2, pages 257–262, October 2004
How to Cite
Maragos, W. F. and Korde, A. S. (2004), Mitochondrial uncoupling as a potential therapeutic target in acute central nervous system injury. Journal of Neurochemistry, 91: 257–262. doi: 10.1111/j.1471-4159.2004.02736.x
- Issue published online: 17 SEP 2004
- Article first published online: 17 SEP 2004
- Received June 10, 2004; accepted July 11, 2004.
- membrane potential;
- reactive oxygen species
Mitochondrial dysfunction, resulting from the disruption of calcium homeostasis and the generation of toxic reactive oxygen species, is a central process leading to neuronal injury and death following acute CNS insults. Interventions aimed at preventing disturbances in mitochondrial function have therefore become targets of intense investigation. Mitochondrial uncoupling is a condition in which electron transport is disconnected from the production of ATP. As a consequence, there is a decrease in the mitochondrial membrane potential, which can temporarily decrease calcium influx and attenuate free radical formation. The potential use of pharmacological agents with uncoupling properties may provide a novel therapeutic approach for the treatment of acute neuronal injury.