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

Jordan Rose, Christian Brian, Jade Woods, Aglaia Pappa, Mihalis I. Panayiotidis, Robert Powers, Rodrigo Franco

Research output: Contribution to journalArticle

29 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)109-115
Number of pages7
JournalToxicology
Volume391
DOIs
StatePublished - Nov 1 2017

Keywords

  • Astrocytes
  • Calcium
  • Free fatty acid oxidation
  • Glycolysis
  • Inflammation
  • Microglia
  • Mitochondria
  • Oligodendrocytes
  • Redox

ASJC Scopus subject areas

  • Toxicology

Fingerprint Dive into the research topics of 'Mitochondrial dysfunction in glial cells: Implications for neuronal homeostasis and survival'. Together they form a unique fingerprint.

  • Cite this