Mitochondrial Dysfunction in Glial Cells: Implications for Neuronal Homeostasis and Survival

Jordan Rose, Christian Brian, Jade Woods, Aglaia Pappa, Mihalis Panagiotidis, Robert Powers, Rodrigo Franco

Research output: Contribution to journalArticlepeer-review

42 Citations (Scopus)
5 Downloads (Pure)

Abstract

Mitochondrial dysfunction is central to the pathogenesis of neurological disorders. Neurons rely on oxidative phosphorylation to meet their energy requirements and thus alterations in mitochondrial function are linked to energy failure and neuronal cell death. Furthermore, dysfunctional mitochondria are reported to increase the steady-state levels of reactive oxygen species derived from the leakage of electrons from the electron transport chain. Research aimed at understanding mitochondrial dysfunction and its role in neurological disorders has been primarily geared towards neurons. In contrast, the role that dysfunctional mitochondria have in glial cells’ function and its implication for neuronal homeostasis and brain function has been largely understudied. Except for oligodendrocytes, astrocytes and microglia do not degenerate upon the impairment of mitochondrial function, as they rely primarily on glycolysis to produce energy and have a higher antioxidant capacity than neurons. However, recent evidence highlights the role of mitochondrial metabolism and signaling in glial cell function. In this work, we review the functional role of mitochondria in glial cells and the evidence regarding its potential role regulating neuronal homeostasis and disease progression.
Original languageEnglish
Pages (from-to)109-115
JournalToxicology
Volume391
Early online date26 Jun 2017
DOIs
Publication statusPublished - 1 Nov 2017

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