Autophagy in Myelinating Glia.
Journal
The Journal of neuroscience : the official journal of the Society for Neuroscience
ISSN: 1529-2401
Titre abrégé: J Neurosci
Pays: United States
ID NLM: 8102140
Informations de publication
Date de publication:
08 01 2020
08 01 2020
Historique:
received:
28
05
2019
revised:
17
10
2019
accepted:
08
11
2019
pubmed:
21
11
2019
medline:
14
7
2020
entrez:
21
11
2019
Statut:
ppublish
Résumé
Autophagy is the cellular process involved in transportation and degradation of membrane, proteins, pathogens, and organelles. This fundamental cellular process is vital in development, plasticity, and response to disease and injury. Compared with neurons, little information is available on autophagy in glia, but it is paramount for glia to perform their critical responses to nervous system disease and injury, including active tissue remodeling and phagocytosis. In myelinating glia, autophagy has expanded roles, particularly in phagocytosis of mature myelin and in generating the vast amounts of membrane proteins and lipids that must be transported to form new myelin. Notably, autophagy plays important roles in removing excess cytoplasm to promote myelin compaction and development of oligodendrocytes, as well as in remyelination by Schwann cells after nerve trauma. This review summarizes the cell biology of autophagy, detailing the major pathways and proteins involved, as well as the roles of autophagy in Schwann cells and oligodendrocytes in development, plasticity, and diseases in which myelin is affected. This includes traumatic brain injury, Alexander's disease, Alzheimer's disease, hypoxia, multiple sclerosis, hereditary spastic paraplegia, and others. Promising areas for future research are highlighted.
Identifiants
pubmed: 31744863
pii: JNEUROSCI.1066-19.2019
doi: 10.1523/JNEUROSCI.1066-19.2019
pmc: PMC6948934
doi:
Types de publication
Journal Article
Research Support, N.I.H., Intramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
256-266Subventions
Organisme : Intramural NIH HHS
ID : ZIA HD000713
Pays : United States
Organisme : Intramural NIH HHS
ID : ZIA HD001607
Pays : United States
Informations de copyright
Copyright © 2020 the authors.
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