Evidence map›Paper›PMID 29114067›Full record

ReviewThe Journal of cell biology2017

Regulation and dysregulation of axon infrastructure by myelinating glia.

Simon Pan, Jonah R Chan

Open access · bronzeAbstract readReview
In one paragraph

Review in The Journal of cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Diabetic neuropathy: cutting-edge research and future directions.Signal transduction and targeted therapy · 2025
    Review
  3. Maladaptive Peripheral Ketogenesis in Schwann Cells Mediated by CBAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Blockage of MLKL prevents myelin damage in experimental diabetic neuropathy.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. The Current Challenges for Drug Discovery in CNS Remyelination.International journal of molecular sciences · 2021
    Review
  17. Review
  18. Review
  19. Article
  20. Article
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

2 authors at 1 institution in 1 country.

Simon PanDepartment of Neurology, University of California, San Francisco, San Francisco, CA simon.pan@ucsf.edu.ORCID 0000-0002-0207-1617
Jonah R ChanDepartment of Neurology, University of California, San Francisco, San Francisco, CA.ORCID 0000-0002-2176-1242
University of California, San Francisco · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007618 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ANDERSON, MARK S · 1985 to 2020
$29.6M
THE ESTABLISHMENT OF SCHWANN CELL POLARITY AND THE INITIATION OF MYELINATIONR01NS062796 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHAN, JONAH R · 2008 to 2018
$3.4M
Functional Screening of GPCR Small Molecule Libraries for Remyelination TherapiesR01NS095889 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAN, JONAH R · 2016 to 2020
$1.9M
Somatodendritic Inhibition of Oligodendrocyte MyelinationR01NS097428 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHAN, JONAH R, PELES, ELIOR · 2016 to 2020
$1.5M
NIGMS NIH HHS T32 GM007618NINDS NIH HHS R01 NS062796NINDS NIH HHS R01 NS095889NINDS NIH HHS R01 NS097428
6 · The paper itself

Abstract

Axon loss and neurodegeneration constitute clinically debilitating sequelae in demyelinating diseases such as multiple sclerosis, but the underlying mechanisms of secondary degeneration are not well understood. Myelinating glia play a fundamental role in promoting the maturation of the axon cytoskeleton, regulating axon trafficking parameters, and imposing architectural rearrangements such as the nodes of Ranvier and their associated molecular domains. In the setting of demyelination, these changes may be reversed or persist as maladaptive features, leading to axon degeneration. In this review, we consider recent insights into axon-glial interactions during development and disease to propose that disruption of the cytoskeleton, nodal architecture, and other components of axon infrastructure is a potential mediator of pathophysiological damage after demyelination.

Indexed as

AnimalsAxonsCell Adhesion Molecules, NeuronalContactin 1CytoskeletonDemyelinating DiseasesGene Expression RegulationHumansIon ChannelsMiceMyelin SheathNeurodegenerative DiseasesSignal TransductionSpectrinCell Adhesion Molecules, NeuronalCntn1 protein, mouseCntnap1 protein, mouseContactin 1Ion ChannelsSpectrin

Identifiers

PMID29114067
PMCPMC5716274
OpenAlexW2767612966

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.