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 language | English (US) |
|---|---|
| Pages (from-to) | 109-115 |
| Number of pages | 7 |
| Journal | Toxicology |
| Volume | 391 |
| DOIs | |
| State | Published - Nov 1 2017 |
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Keywords
- Astrocytes
- Calcium
- Free fatty acid oxidation
- Glycolysis
- Inflammation
- Microglia
- Mitochondria
- Oligodendrocytes
- Redox
ASJC Scopus subject areas
- Toxicology
Cite this
Mitochondrial dysfunction in glial cells : Implications for neuronal homeostasis and survival. / Rose, Jordan; Brian, Christian; Woods, Jade; Pappa, Aglaia; Panayiotidis, Mihalis I.; Powers, Robert; Franco-Cruz, Rodrigo.
In: Toxicology, Vol. 391, 01.11.2017, p. 109-115.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Mitochondrial dysfunction in glial cells
T2 - Implications for neuronal homeostasis and survival
AU - Rose, Jordan
AU - Brian, Christian
AU - Woods, Jade
AU - Pappa, Aglaia
AU - Panayiotidis, Mihalis I.
AU - Powers, Robert
AU - Franco-Cruz, Rodrigo
PY - 2017/11/1
Y1 - 2017/11/1
N2 - 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.
AB - 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.
KW - Astrocytes
KW - Calcium
KW - Free fatty acid oxidation
KW - Glycolysis
KW - Inflammation
KW - Microglia
KW - Mitochondria
KW - Oligodendrocytes
KW - Redox
UR - http://www.scopus.com/inward/record.url?scp=85026649944&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85026649944&partnerID=8YFLogxK
U2 - 10.1016/j.tox.2017.06.011
DO - 10.1016/j.tox.2017.06.011
M3 - Article
C2 - 28655545
AN - SCOPUS:85026649944
VL - 391
SP - 109
EP - 115
JO - Toxicology
JF - Toxicology
SN - 0300-483X
ER -