Evidence map›Paper›PMID 31744863›Full record

ReviewThe Journal of neuroscience : the official journal of the Society for Neuroscience2020

Autophagy in Myelinating Glia.

Jillian Belgrad, Raffaella De Pace, R Douglas Fields

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.5field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. White matter injury after brain ischemia.Experimental neurology · 2026
    Review
  3. Review
  4. Deletion of murineScience translational medicine · 2025
    Article
  5. Article
  6. Review
  7. TMEM63A, associated with hypomyelinating leukodystrophies, is an evolutionarily conserved regulator of myelination.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Epigenetic regulation ofAutophagy · 2024
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 2 countries.

Jillian BelgradSection on Nervous System Development and Plasticity and.
Raffaella De PaceSection on Intracellular Protein Trafficking, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892.ORCID 0000-0002-8179-6869
R Douglas FieldsSection on Nervous System Development and Plasticity and fieldsd@mail.nih.gov.
National Institutes of Health · USSchool for Field Studies · USThe Enteric Nervous System in Gut and Brain Disorders · FR

Funding

Protein Trafficking In The Endosomal-Lysosomal SystemZIAHD001607 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI BONIFACINO, JUAN · 2009 to 2025
$48.3M
Nervous System Development and PlasticityZIAHD000713 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI FIELDS, RICHARD DOUGLAS · 2009 to 2023
$17.7M
Intramural NIH HHS ZIA HD000713Intramural NIH HHS ZIA HD001607
6 · The paper itself

Abstract

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.

Indexed as

AnimalsAutophagyHumansMyelin SheathNeuroglia

Identifiers

PMID31744863
PMCPMC6948934
OpenAlexW2991551920

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.