Evidence map›Paper›PMID 25364952›Full record

ReviewCurrent opinion in neurology2014

The back and forth of axonal injury and repair after stroke.

Jason D Hinman

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 9% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. White matter injury after brain ischemia.Experimental neurology · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Spatiotemporal transcriptomic map of glial cell response in a mouse model of acute brain ischemia.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  12. Synaptotagmin 4 Supports Spontaneous Axon Sprouting after Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  13. Article
  14. Motor Activity-Induced White Matter Repair in White Matter Stroke.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  15. Article
  16. Role of NADCellular and molecular neurobiology · 2023
    Review
  17. Article
  18. Review
  19. Review
  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

1 author at 1 institution in 1 country.

Jason D HinmanDepartment of Neurology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA.
University of California, Los Angeles · US

Funding

Molecular Mechanisms of Axonal Degeneration After White Matter StrokeK08NS083740 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI HINMAN, JASON D · 2013 to 2017
$831k
NINDS NIH HHS K08 NS083740NINDS NIH HHS L30 NS080243
6 · The paper itself

Abstract

purpose of reviewThe axon plays a central role in both the injury and repair phases after stroke. This review highlights emerging principles in the study of axonal injury in stroke and the role of the axon in neural repair after stroke. RECENT

findingsIschemic stroke produces a rapid and significant loss of axons in the acute phase. This early loss of axons results from a primary ischemic injury that triggers a wave of calcium signaling, activating proteolytic mechanisms and downstream signaling cascades. A second progressive phase of axonal injury occurs during the subacute period and damages axons that survive the initial ischemic insult but go on to experience a delayed axonal degeneration driven in part by changes in axoglial contact and axonal energy metabolism. Recovery from stroke is dependent on axonal sprouting and reconnection that occurs during a third degenerative/regenerative phase. Despite this central role played by the axon, comparatively little is understood about the molecular pathways that contribute to early and subacute axonal degeneration after stroke. Recent advances in axonal neurobiology and signaling suggest new targets that hold promise as potential molecular therapeutics including axonal calcium signaling, axoglial energy metabolism and cell adhesion as well as retrograde axonal mitogen-activated protein kinase pathways. These novel pathways must be modeled appropriately as the type and severity of axonal injury vary by stroke subtype. SUMMARY: Stroke-induced injury to axons occurs in three distinct phases each with a unique molecular underpinning. A wealth of new data about the molecular organization and molecular signaling within axons is available but not yet robustly applied to the study of axonal injury after stroke. Identifying the spatiotemporal patterning of molecular pathways within the axon that contribute to injury and repair may offer new therapeutic strategies for the treatment of stroke.

Indexed as

AnimalsAxonsHumansNerve DegenerationNerve RegenerationSignal TransductionStroke

Identifiers

PMID25364952
PMCPMC4459741
OpenAlexW2316296639

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.