TY - JOUR
T1 - Astrocyte Mitochondria in White-Matter Injury
AU - Nguyen, Hung
AU - Zerimech, Sarah
AU - Baltan, Selva
N1 - Publisher Copyright:
© 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature.
PY - 2021/10
Y1 - 2021/10
N2 - This review summarizes the diverse structure and function of astrocytes to describe the bioenergetic versatility required of astrocytes that are situated at different locations. The intercellular domain of astrocyte mitochondria defines their roles in supporting and regulating astrocyte-neuron coupling and survival against ischemia. The heterogeneity of astrocyte mitochondria, and how subpopulations of astrocyte mitochondria adapt to interact with other glia and regulate axon function, require further investigation. It has become clear that mitochondrial permeability transition pores play a key role in a wide variety of human diseases, whose common pathology may be based on mitochondrial dysfunction triggered by Ca2+ and potentiated by oxidative stress. Reactive oxygen species cause axonal degeneration and a reduction in axonal transport, leading to axonal dystrophies and neurodegeneration including Alzheimer’s disease, amyotrophic lateral sclerosis, Parkinson’s disease, and Huntington’s disease. Developing new tools to allow better investigation of mitochondrial structure and function in astrocytes, and techniques to specifically target astrocyte mitochondria, can help to unravel the role of mitochondrial health and dysfunction in a more inclusive context outside of neuronal cells. Overall, this review will assess the value of astrocyte mitochondria as a therapeutic target to mitigate acute and chronic injury in the CNS.
AB - This review summarizes the diverse structure and function of astrocytes to describe the bioenergetic versatility required of astrocytes that are situated at different locations. The intercellular domain of astrocyte mitochondria defines their roles in supporting and regulating astrocyte-neuron coupling and survival against ischemia. The heterogeneity of astrocyte mitochondria, and how subpopulations of astrocyte mitochondria adapt to interact with other glia and regulate axon function, require further investigation. It has become clear that mitochondrial permeability transition pores play a key role in a wide variety of human diseases, whose common pathology may be based on mitochondrial dysfunction triggered by Ca2+ and potentiated by oxidative stress. Reactive oxygen species cause axonal degeneration and a reduction in axonal transport, leading to axonal dystrophies and neurodegeneration including Alzheimer’s disease, amyotrophic lateral sclerosis, Parkinson’s disease, and Huntington’s disease. Developing new tools to allow better investigation of mitochondrial structure and function in astrocytes, and techniques to specifically target astrocyte mitochondria, can help to unravel the role of mitochondrial health and dysfunction in a more inclusive context outside of neuronal cells. Overall, this review will assess the value of astrocyte mitochondria as a therapeutic target to mitigate acute and chronic injury in the CNS.
KW - Astroglial interactions
KW - Axonal degeneration
KW - Glial cells
KW - Mitochondrial dynamics
KW - Neurodegenerative diseases
KW - Neurovascular injuries
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U2 - 10.1007/s11064-021-03239-8
DO - 10.1007/s11064-021-03239-8
M3 - Article
C2 - 33527218
AN - SCOPUS:85100121886
SN - 0364-3190
VL - 46
SP - 2696
EP - 2714
JO - Neurochemical Research
JF - Neurochemical Research
IS - 10
ER -