Evidence map›Paper›PMID 34151767›Full record

ArticleCurrent neuropharmacology2022

Pathways Involved in Remyelination after Cerebral Ischemia.

Gonzalo Garcia-Martin, Berta Alcover-Sanchez, Francisco Wandosell, Beatriz Cubelos

Abstract read
In one paragraph

Article in Current neuropharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing 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

21 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Inhibition of SCFCommunications biology · 2025
    Article
  10. Article
  11. Blood-brain barrier breakdown in brain ischemia: Insights from MRI perfusion imaging.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  12. Article
  13. Article
  14. HMolecular neurobiology · 2023
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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.

Gonzalo Garcia-MartinDepartamento de Biología Molecular and Centro Biología Molecular "Severo Ochoa", Universidad Autónoma de Madrid-Consejo Superior de Investigaciones Científicas, 28049 Madrid, Spain.
Berta Alcover-SanchezDepartamento de Biología Molecular and Centro Biología Molecular "Severo Ochoa", Universidad Autónoma de Madrid-Consejo Superior de Investigaciones Científicas, 28049 Madrid, Spain.
Francisco WandosellDepartamento de Biología Molecular and Centro Biología Molecular "Severo Ochoa", Universidad Autónoma de Madrid-Consejo Superior de Investigaciones Científicas, 28049 Madrid, Spain.
Beatriz CubelosDepartamento de Biología Molecular and Centro Biología Molecular "Severo Ochoa", Universidad Autónoma de Madrid-Consejo Superior de Investigaciones Científicas, 28049 Madrid, Spain.

Funding

Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) PI2016/01Comunidad de Madrid CAM-Biomedicina B2017/BMD-3700Spanish Ministry of Economy and Competitiveness RTI2018-096303B-C33, RTI2018-096303-B-C1
6 · The paper itself

Abstract

Brain ischemia, also known as ischemic stroke, occurs when there is a lack of blood supply into the brain. When an ischemic insult appears, both neurons and glial cells can react in several ways that will determine the severity and prognosis. This high heterogeneity of responses has been a major obstacle in developing effective treatments or preventive methods for stroke. Although white matter pathophysiology has not been deeply assessed in stroke, its remodelling can greatly influence the clinical outcome and the disability degree. Oligodendrocytes, the unique cell type implied in CNS myelination, are sensible to ischemic damage. Loss of myelin sheaths can compromise axon survival, so new Oligodendrocyte Precursor Cells are required to restore brain function. Stroke can, therefore, enhance oligodendrogenesis to regenerate those new oligodendrocytes that will ensheath the damaged axons. Given that myelination is a highly complex process that requires coordination of multiple pathways such as Sonic Hedgehog, RTKs or Wnt/β-catenin, we will analyse new research highlighting their importance after brain ischemia. In addition, oligodendrocytes are not isolated cells inside the brain, but rather form part of a dynamic environment of interactions between neurons and glial cells. For this reason, we will put some context into how microglia and astrocytes react against stroke and influence oligodendrogenesis to highlight the relevance of remyelination in the ischemic brain. This will help to guide future studies to develop treatments focused on potentiating the ability of the brain to repair the damage.

Indexed as

Brain IschemiaRemyelinationStrokeHedgehog ProteinsHumansOligodendrogliaHedgehog ProteinsCerebral ischemiaglial cellsoligodendrocyteoligodendrocyte precursor cellremyelinationstroke

Identifiers

PMID34151767
PMCPMC9878953

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.