Neuroinflammation in Acute Ischemic and Hemorrhagic Stroke.
Astrocytes
Brain damage
Chemokines
Cytokines
Edema
Glial cells
Hemorrhagic stroke
Immune cells
Inflammatory response
Intracerebral hemorrhage
Ischemic stroke
Microglia
Neuroinflammation
Pathophysiology
Secondary injury
Therapeutic targets
Journal
Current neurology and neuroscience reports
ISSN: 1534-6293
Titre abrégé: Curr Neurol Neurosci Rep
Pays: United States
ID NLM: 100931790
Informations de publication
Date de publication:
08 2023
08 2023
Historique:
accepted:
24
05
2023
pmc-release:
01
08
2024
medline:
28
7
2023
pubmed:
3
7
2023
entrez:
3
7
2023
Statut:
ppublish
Résumé
This review aims to provide an overview of neuroinflammation in ischemic and hemorrhagic stroke, including recent findings on the mechanisms and cellular players involved in the inflammatory response to brain injury. Neuroinflammation is a crucial process following acute ischemic stroke (AIS) and hemorrhagic stroke (HS). In AIS, neuroinflammation is initiated within minutes of the ischemia onset and continues for several days. In HS, neuroinflammation is initiated by blood byproducts in the subarachnoid space and/or brain parenchyma. In both cases, neuroinflammation is characterized by the activation of resident immune cells, such as microglia and astrocytes, and infiltration of peripheral immune cells, leading to the release of pro-inflammatory cytokines, chemokines, and reactive oxygen species. These inflammatory mediators contribute to blood-brain barrier disruption, neuronal damage, and cerebral edema, promoting neuronal apoptosis and impairing neuroplasticity, ultimately exacerbating the neurologic deficit. However, neuroinflammation can also have beneficial effects by clearing cellular debris and promoting tissue repair. The role of neuroinflammation in AIS and ICH is complex and multifaceted, and further research is necessary to develop effective therapies that target this process. Intracerebral hemorrhage (ICH) will be the HS subtype addressed in this review. Neuroinflammation is a significant contributor to brain tissue damage following AIS and HS. Understanding the mechanisms and cellular players involved in neuroinflammation is essential for developing effective therapies to reduce secondary injury and improve stroke outcomes. Recent findings have provided new insights into the pathophysiology of neuroinflammation, highlighting the potential for targeting specific cytokines, chemokines, and glial cells as therapeutic strategies.
Identifiants
pubmed: 37395873
doi: 10.1007/s11910-023-01282-2
pii: 10.1007/s11910-023-01282-2
pmc: PMC10544736
mid: NIHMS1931757
doi:
Substances chimiques
Cytokines
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
407-431Subventions
Organisme : NINDS NIH HHS
ID : R21 NS130423
Pays : United States
Informations de copyright
© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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