Literature DB >> 28655545

Mitochondrial dysfunction in glial cells: Implications for neuronal homeostasis and survival.

Jordan Rose1, Christian Brian2, Jade Woods3, Aglaia Pappa4, Mihalis I Panayiotidis5, Robert Powers6, Rodrigo Franco7.   

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, in neurons, 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 effects of mitochondrial dysfunction in glial cells' function and its implication for neuronal homeostasis and brain function has been largely understudied. Unlike neurons and 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.
Copyright © 2017 Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Astrocytes; Calcium; Free fatty acid oxidation; Glycolysis; Inflammation; Microglia; Mitochondria; Oligodendrocytes; Redox

Mesh:

Year:  2017        PMID: 28655545      PMCID: PMC5681369          DOI: 10.1016/j.tox.2017.06.011

Source DB:  PubMed          Journal:  Toxicology        ISSN: 0300-483X            Impact factor:   4.221


  76 in total

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