Evidence map›Paper›PMID 27566737›Full record

ReviewTranslational stroke research2017

Mechanisms of Axonal Damage and Repair after Central Nervous System Injury.

Naohiro Egawa, Josephine Lok, Kazuo Washida, Ken Arai

Abstract readReview
In one paragraph

Review in Translational stroke research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
–field-weighted citation impact
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

45 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Disease markers · 2022
    Article
  14. Article
  15. One Raft to Guide Them All, and in Axon Regeneration Inhibit Them.International journal of molecular sciences · 2021
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. From in vitro to in vivo reprogramming for neural transdifferentiation: An approach for CNS tissue remodeling using stem cell technology.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
    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

4 authors.

Naohiro EgawaNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, MGH East 149-2401, Charlestown, MA, 02129, USA.
Josephine LokNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, MGH East 149-2401, Charlestown, MA, 02129, USA.
Kazuo WashidaNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, MGH East 149-2401, Charlestown, MA, 02129, USA.
Ken AraiNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, MGH East 149-2401, Charlestown, MA, 02129, USA. karai@partners.org.

Funding

Targeting ROCK for Neurogliovascular Plasticity & Remodeling After StrokeP01NS055104 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI LO, ENG H. · 2007 to 2018
$13.3M
Oligo-Vascular Signaling in StrokeR01NS065089 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ARAI, KEN · 2010 to 2019
$3.8M
NINDS NIH HHS P01 NS055104NINDS NIH HHS R01 NS065089
6 · The paper itself

Abstract

Central nervous system (CNS) injury initiates spatial and temporal neurodegeneration. Under pathologic conditions, damaged glial cells cannot supply sufficient metabolites to neurons, leading to energy deficiency for neuronal axons. The widespread disruption of cellular membranes causes disturbed intracellular signaling via dysregulated ionic gradients in neurons. Although several deleterious cascades are activated during the acute phase of CNS injury, some compensatory responses may tend to promote axonal repair during the chronic/remodeling phase. Because it may not be easy to block all multifactorial neurodegenerative pathways after CNS injury, supporting or boosting endogenous regenerative mechanisms would be an important therapeutic approach for CNS diseases. In this mini-review, we briefly but broadly introduce basic mechanisms that trigger axonal degeneration and then discuss potential targets for promoting axonal regeneration after CNS injury.

Indexed as

RegenerationAnimalsApoptosisAxonsCentral Nervous SystemHumansMyelin SheathNeurogliaSignal TransductionAxonal regenerationAxonal repairCNS injury

Identifiers

PMID27566737
PMCPMC5243173

What OpenQuestion holds

Textmetadata
LicenceTDM
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.