Abstract
Neuroinflammatory mediators play a crucial role in the pathophysiology of brain ischemia, exerting either deleterious effects on the progression of tissue damage or beneficial roles during recovery and repair. Within hours after the ischemic insult, increased levels of cytokines and chemokines enhance the expression of adhesion molecules on cerebral endothelial cells, facilitating the adhesion and transendothelial migration of circulating neutrophils and monocytes. These cells may accumulate in the capillaries, further impairing cerebral blood flow, or extravasate into the brain parenchyma. Infiltrating leukocytes, as well as resident brain cells, including neurons and glia, may release pro-inflammatory mediators, such as cytokines, chemokines and oxygen/nitrogen free radicals that contribute to the evolution of tissue damage. Moreover, recent studies have highlighted the involvement of matrix metalloproteinases in the propagation and regulation of neuroinflammatory responses to ischemic brain injury. These enzymes cleave protein components of the extracellular matrix such as collagen, proteoglycan and laminin, but also process a number of cell-surface and soluble proteins, including receptors and cytokines such as interleukin-1β. The present work reviewed the role of neuroinflammatory mediators in the pathophysiology of ischemic brain damage and their potential exploitation as drug targets for the treatment of cerebral ischemia.
| Original language | English |
|---|---|
| Pages (from-to) | 13-26 |
| Number of pages | 14 |
| Journal | FEBS Journal |
| Volume | 276 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Jan 2009 |
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Keywords
- Brain ischemia
- Cytokines
- Matrix metalloproteinases
- Microglia
- Neuroinflammation
ASJC Scopus subject areas
- Biochemistry
- Cell Biology
- Molecular Biology
Cite this
Post-ischemic brain damage : Pathophysiology and role of inflammatory mediators. / Amantea, Diana; Nappi, Giuseppe; Bernardi, Giorgio; Bagetta, Giacinto; Corasaniti, Maria T.
In: FEBS Journal, Vol. 276, No. 1, 01.2009, p. 13-26.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Post-ischemic brain damage
T2 - Pathophysiology and role of inflammatory mediators
AU - Amantea, Diana
AU - Nappi, Giuseppe
AU - Bernardi, Giorgio
AU - Bagetta, Giacinto
AU - Corasaniti, Maria T.
PY - 2009/1
Y1 - 2009/1
N2 - Neuroinflammatory mediators play a crucial role in the pathophysiology of brain ischemia, exerting either deleterious effects on the progression of tissue damage or beneficial roles during recovery and repair. Within hours after the ischemic insult, increased levels of cytokines and chemokines enhance the expression of adhesion molecules on cerebral endothelial cells, facilitating the adhesion and transendothelial migration of circulating neutrophils and monocytes. These cells may accumulate in the capillaries, further impairing cerebral blood flow, or extravasate into the brain parenchyma. Infiltrating leukocytes, as well as resident brain cells, including neurons and glia, may release pro-inflammatory mediators, such as cytokines, chemokines and oxygen/nitrogen free radicals that contribute to the evolution of tissue damage. Moreover, recent studies have highlighted the involvement of matrix metalloproteinases in the propagation and regulation of neuroinflammatory responses to ischemic brain injury. These enzymes cleave protein components of the extracellular matrix such as collagen, proteoglycan and laminin, but also process a number of cell-surface and soluble proteins, including receptors and cytokines such as interleukin-1β. The present work reviewed the role of neuroinflammatory mediators in the pathophysiology of ischemic brain damage and their potential exploitation as drug targets for the treatment of cerebral ischemia.
AB - Neuroinflammatory mediators play a crucial role in the pathophysiology of brain ischemia, exerting either deleterious effects on the progression of tissue damage or beneficial roles during recovery and repair. Within hours after the ischemic insult, increased levels of cytokines and chemokines enhance the expression of adhesion molecules on cerebral endothelial cells, facilitating the adhesion and transendothelial migration of circulating neutrophils and monocytes. These cells may accumulate in the capillaries, further impairing cerebral blood flow, or extravasate into the brain parenchyma. Infiltrating leukocytes, as well as resident brain cells, including neurons and glia, may release pro-inflammatory mediators, such as cytokines, chemokines and oxygen/nitrogen free radicals that contribute to the evolution of tissue damage. Moreover, recent studies have highlighted the involvement of matrix metalloproteinases in the propagation and regulation of neuroinflammatory responses to ischemic brain injury. These enzymes cleave protein components of the extracellular matrix such as collagen, proteoglycan and laminin, but also process a number of cell-surface and soluble proteins, including receptors and cytokines such as interleukin-1β. The present work reviewed the role of neuroinflammatory mediators in the pathophysiology of ischemic brain damage and their potential exploitation as drug targets for the treatment of cerebral ischemia.
KW - Brain ischemia
KW - Cytokines
KW - Matrix metalloproteinases
KW - Microglia
KW - Neuroinflammation
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U2 - 10.1111/j.1742-4658.2008.06766.x
DO - 10.1111/j.1742-4658.2008.06766.x
M3 - Article
C2 - 19087196
AN - SCOPUS:57649186797
VL - 276
SP - 13
EP - 26
JO - FEBS Journal
JF - FEBS Journal
SN - 1742-464X
IS - 1
ER -