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Oxidative Medicine and Cellular Longevity
Volume 2013, Article ID 194546, 13 pages
Review Article

Targeting Microglial KATP Channels to Treat Neurodegenerative Diseases: A Mitochondrial Issue

1Unitat de Bioquímica i Biologia Molecular, Facultat de Medicina, Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), UB c/Casanova 143, E 08036 Barcelona, Spain
2Neurometabolic Disease Lab, Hospital Duran i Reynals, L'Hospitalet de Llobregat, E 08907 Barcelona, Spain

Received 14 January 2013; Revised 26 March 2013; Accepted 8 May 2013

Academic Editor: Grzegorz A. Czapski

Copyright © 2013 Manuel J. Rodríguez et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Neurodegeneration is a complex process involving different cell types and neurotransmitters. A common characteristic of neurodegenerative disorders is the occurrence of a neuroinflammatory reaction in which cellular processes involving glial cells, mainly microglia and astrocytes, are activated in response to neuronal death. Microglia do not constitute a unique cell population but rather present a range of phenotypes closely related to the evolution of neurodegeneration. In a dynamic equilibrium with the lesion microenvironment, microglia phenotypes cover from a proinflammatory activation state to a neurotrophic one directly involved in cell repair and extracellular matrix remodeling. At each moment, the microglial phenotype is likely to depend on the diversity of signals from the environment and of its response capacity. As a consequence, microglia present a high energy demand, for which the mitochondria activity determines the microglia participation in the neurodegenerative process. As such, modulation of microglia activity by controlling microglia mitochondrial activity constitutes an innovative approach to interfere in the neurodegenerative process. In this review, we discuss the mitochondrial KATP channel as a new target to control microglia activity, avoid its toxic phenotype, and facilitate a positive disease outcome.