Evidence map›Paper›PMID 34208834›Full record

ReviewCells2021

Glial Cells as Therapeutic Approaches in Brain Ischemia-Reperfusion Injury.

Ivó H Hernández, Mario Villa-González, Gerardo Martín, Manuel Soto, María José Pérez-Álvarez

Abstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 2 pooled it
–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

56 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
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  6. Mitochondria transfer in tissue homeostasis and diseases.International journal of biological sciences · 2026
    Review
  7. Review
  8. Review
  9. Physical mechanisms of human brain functions.Quantitative biology (Beijing, China) · 2025
    Review
  10. The effects of self-assembling peptide on glial cell activation.Naunyn-Schmiedeberg's archives of pharmacology · 2025
    Review
  11. Article
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  14. Article
  15. Article
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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

5 authors.

Ivó H HernándezGenomic Instability Group, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain.ORCID 0000-0001-9656-6508
Mario Villa-GonzálezCenter for Molecular Biology "Severo Ochoa" (CBMSO) UAM/CSIC, 28049 Madrid, Spain.ORCID 0000-0003-4590-5498
Gerardo MartínDepartamento de Biología (Fisiología Animal), Facultad de Ciencias, Universidad Autónoma de Madrid, 28049 Madrid, Spain.ORCID 0000-0001-7769-0829
Manuel SotoCenter for Molecular Biology "Severo Ochoa" (CBMSO) UAM/CSIC, 28049 Madrid, Spain.
María José Pérez-ÁlvarezCenter for Molecular Biology "Severo Ochoa" (CBMSO) UAM/CSIC, 28049 Madrid, Spain.ORCID 0000-0001-8334-8085

Funding

Departamento de Biología, Facultad de Ciencias-UAM BIOUAM03-2020Universidad Autónoma de Madrid Ayudas para el fomento de la investigación en estudios de Máster-UAM 2020
6 · The paper itself

Abstract

Ischemic stroke is the second cause of mortality and the first cause of long-term disability constituting a serious socioeconomic burden worldwide. Approved treatments include thrombectomy and rtPA intravenous administration, which, despite their efficacy in some cases, are not suitable for a great proportion of patients. Glial cell-related therapies are progressively overcoming inefficient neuron-centered approaches in the preclinical phase. Exploiting the ability of microglia to naturally switch between detrimental and protective phenotypes represents a promising therapeutic treatment, in a similar way to what happens with astrocytes. However, the duality present in many of the roles of these cells upon ischemia poses a notorious difficulty in disentangling the precise pathways to target. Still, promoting M2/A2 microglia/astrocyte protective phenotypes and inhibiting M1/A1 neurotoxic profiles is globally rendering promising results in different in vivo models of stroke. On the other hand, described oligodendrogenesis after brain ischemia seems to be strictly beneficial, although these cells are the less studied players in the stroke paradigm and negative effects could be described for oligodendrocytes in the next years. Here, we review recent advances in understanding the precise role of mentioned glial cell types in the main pathological events of ischemic stroke, including inflammation, blood brain barrier integrity, excitotoxicity, reactive oxygen species management, metabolic support, and neurogenesis, among others, with a special attention to tested therapeutic approaches.

Indexed as

AnimalsBlood-Brain BarrierBrain IschemiaHumansNeurogenesisNeurogliaOxidative StressReperfusion Injuryastrocytesgliaischemic strokemicroglianeuroprotectionoligodendrocytestherapy

Identifiers

PMID34208834
PMCPMC8305833

What OpenQuestion holds

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Registered trials

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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.