Inflammatory Responses in Brain Ischemia
Top Cited Papers
- 11 March 2015
- journal article
- review article
- Published by Bentham Science Publishers Ltd. in Current Medicinal Chemistry
- Vol. 22 (10), 1258-1277
- https://doi.org/10.2174/0929867322666150209154036
Abstract
Abstract: Brain infarction causes tissue death by ischemia due to occlusion of the cerebral vessels and recent work has shown that post stroke inflammation contributes significantly to the development of ischemic pathology. Because secondary damage by brain inflammation may have a longer therapeutic time window compared to the rescue of primary damage following arterial occlusion, controlling inflammation would be an obvious therapeutic target. A substantial amount of experimentall progress in this area has been made in recent years. However, it is difficult to elucidate the precise mechanisms of the inflammatory responses following ischemic stroke because inflammation is a complex series of interactions between inflammatory cells and molecules, all of which could be either detrimental or beneficial. We review recent advances in neuroinflammation and the modulation of inflammatory signaling pathways in brain ischemia. Potential targets for treatment of ischemic stroke will also be covered. The roles of the immune system and brain damage versus repair will help to clarify how immune modulation may treat stroke.Keywords
This publication has 99 references indexed in Scilit:
- CD18-Mediated Neutrophil Recruitment Contributes to the Pathogenesis of Reperfused but Not Nonreperfused StrokeStroke, 1999
- Mice Deficient in Mac-1 (CD11b/CD18) Are Less Susceptible to Cerebral Ischemia/Reperfusion InjuryStroke, 1999
- Cyclooxygenase‐2 is induced globally in infarcted human brainAnnals of Neurology, 1998
- Matrix Metalloproteinase Expression Increases After Cerebral Focal Ischemia in RatsStroke, 1998
- Tumor Necrosis Factor-αStroke, 1997
- Potentiation of Oxygen-Glucose Deprivation–Induced Neuronal Death After Induction of iNOSStroke, 1996
- E-Selectin Appears in Nonischemic Tissue During Experimental Focal Cerebral IschemiaStroke, 1996
- Anti–Intercellular Adhesion Molecule–1 Antibody Reduces Ischemic Cell Damage After Transient But Not Permanent Middle Cerebral Artery Occlusion in the Wistar RatStroke, 1995
- Interleukin-1 as a Pathogenetic Mediator of Ischemic Brain Damage in RatsStroke, 1995
- Monocyte Chemoattractant Protein–1 Messenger RNA Expression in Rat Ischemic CortexStroke, 1995