Neuroprotective Role of Glial Cells in Cerebral Ischemia

A special issue of Neuroglia (ISSN 2571-6980).

Deadline for manuscript submissions: closed (20 November 2021) | Viewed by 544

Special Issue Editor


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Guest Editor
Institut National de la Santé et de la Recherche (INSERM), Universite Paris 7- Denis Diderot, Paris, France
Interests: cerebral ischemia; neonates; cell death; inflammation; microglia; hemodynamic responses; ultrasound imaging; nitric oxide; prostaglandins

Special Issue Information

Dear Colleagues,

Stroke is a disorder affecting all age groups, particularly those at opposite ends of the age spectrum, with an incidence of 1/2800 to 1/5000 live infant births, and more than 6 million cases every year of adult stroke, respectively. To date, there is still no effective treatment that increases the survival rate or improves the quality of life, both during the neonatal period (the first 28 days of life) and/or in adulthood. During the last decade, the male sex appeared to be a determinant factor, not only in a worse outcome (during the first 40–50 years of life), but also in response to cellular and molecular pathways activated in different cerebral areas involved in behavioral functions.

Stroke triggers dysfunction in several pathways, with multiple final outcomes, which include multiple paths to death or recovery. The activation of resident microglial cells, alongside the infiltration of peripheral macrophages, represents a central inflammatory response to ischemic stroke leading to secondary injury cascade associated with neuronal death.

Microglia/macrophages are the main players in propagating inflammation to tissues neighboring the core site of injury. They perform this task through the production of inflammatory mediators including cytokines and chemokines.

For this Special Issue, we request the submission of manuscripts concerning the molecular pathways in microglia/macrophages and immune cells (infiltration of peripheral myeloid cells including polymorphonuclear cells, lymphocytes, and monocytes), and astrocyte responses after stroke in pre-clinical studies.

Potential topics include:

  • Specific glial genes and region differences between male and female brains;
  • Specific glial responses according to the developmental stage of ischemic animals;
  • Specific glial responses according to rodent species used in stroke models.

These data may highlight the development of additional sex-specific therapeutic strategies in stroke units.

Prof. Dr. Christiane Charriaut-Marlangue
Guest Editor

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Keywords

  • astrocytes
  • microglia
  • cell death
  • M2 phenotype
  • M1 phenotype
  • M-Trans phenotype
  • neonatal ischemia
  • adult ischemia
  • neurovascular unit
  • rat
  • mouse
  • cortex
  • blood–brain barrier
  • female
  • male

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Published Papers

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