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Commentary Open Access
Volume 2 | Issue 1 | DOI: https://doi.org/10.46439/aging.2.008

Astrogliosis after ischemic stroke: Neuroprotection or neuroinflammation?

  • 1Department for Neonatology, Charité University Medical Center, Augustenburger Platz1, 13353 Berlin, Germany
  • 2Neuromuscular Diseases Research Group, Biodonostia Health Research Institute, Paseo Doctor Begiristain, 20014 San Sebastian, Spain
  • 3Department of Physiology, Faculty of Medicine, University of the Basque Country UPV/EHU, Leioa, Spain
+ Affiliations - Affiliations

Corresponding Author

Miren Revuelta, miren.revuelta@ehu.eus

Received Date: February 22, 2021

Accepted Date: March 05, 2021

Abstract

Ischemic stroke is the main cause of disability worldwide affecting around 6 million deaths per year. A cascade of events following the ischemic insult induce energy failure, excitotoxicity and release of inflammatory mediators that provoke cell death and brain injury. In this process, astrocytes undergo a change on gene expression that leads to reactive astrocytes. In this review, different reactive astrocyte populations have been described, in which A1 neurotoxic astrocytes promote a pro-inflammatory environment and reduce neuronal survival, while A2 neuroprotective astrocytes secrete neurotrophic factors and cytokines that promote tissue repair and axonal regeneration. Therapies based on key targets promoting A2 neuroprotective and reducing A1 phenotypes should be further investigated, as they appear to be promising strategies for a clinically successful stroke therapy. 

Keywords

Stroke, Reactive astrocyte, Neuroprotection, Neuroinflammation

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