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NeuroMolecular Medicine

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31.05.2019 | Original Paper

Preserving Mitochondrial Structure and Motility Promotes Recovery of White Matter After Ischemia

verfasst von: Chinthasagar Bastian, Jerica Day, Stephen Politano, John Quinn, Sylvain Brunet, Selva Baltan

Erschienen in: NeuroMolecular Medicine | Ausgabe 4/2019

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Abstract

Stroke significantly affects white matter in the brain by impairing axon function, which results in clinical deficits. Axonal mitochondria are highly dynamic and are transported via microtubules in the anterograde or retrograde direction, depending upon axonal energy demands. Recently, we reported that mitochondrial division inhibitor 1 (Mdivi-1) promotes axon function recovery by preventing mitochondrial fission only when applied during ischemia. Application of Mdivi-1 after injury failed to protect axon function. Interestingly, L-NIO, which is a NOS3 inhibitor, confers post-ischemic protection to axon function by attenuating mitochondrial fission and preserving mitochondrial motility via conserving levels of the microtubular adaptor protein Miro-2. We propose that preventing mitochondrial fission protects axon function during injury, but that restoration of mitochondrial motility is more important to promote axon function recovery after injury. Thus, Miro-2 may be a therapeutic molecular target for recovery following a stroke.

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Titel: Preserving Mitochondrial Structure and Motility Promotes Recovery of White Matter After Ischemia
verfasst von: Chinthasagar Bastian
Jerica Day
Stephen Politano
John Quinn
Sylvain Brunet
Selva Baltan
Publikationsdatum: 31.05.2019
Verlag: Springer US
Erschienen in: NeuroMolecular Medicine / Ausgabe 4/2019
Print ISSN: 1535-1084
Elektronische ISSN: 1559-1174
DOI: https://doi.org/10.1007/s12017-019-08550-w

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Preserving Mitochondrial Structure and Motility Promotes Recovery of White Matter After Ischemia

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