NF-κB and innate immunity in ischemic stroke.
Acute cerebral ischemia elicits an innate immune response that leads to a cascade of events that culminates in necrotic death of neurons and injury to their supportive structures in the neurovascular unit. Indeed, clinical studies have shown a close relationship between elevated levels of inflammatory markers and the risk for ischemic stroke. However, the signaling pathways that link these events are not well understood. A central regulator of inflammatory response is the transcription factor, nuclear factor-kappa B (NF-κB). The activation of NF-κB is required for the transcriptional induction of many proinflammatory mediators involved in innate immunity, such as cellular adhesion molecules, cytokines, and growth factors. Therefore, factors that modulate the activity of NF-κB could potentially regulate inflammatory processes in ischemic stroke. Here, we review the relationship between NF-κB and ischemic stroke, its role in the neurovascular unit, and discuss some animal models that suggest that this relationship is causal.
Harari
Olivier A
OA
Vascular Medicine Research, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Liao
James K
JK
D000818:Animals; D002545:Brain Ischemia / Q000276:immunology*; D004195:Disease Models, Animal; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation / Q000209:etiology / Q000235:genetics / Q000276:immunology; D008959:Models, Neurological; D016328:NF-kappa B / Q000276:immunology*; D015213:Neuroimmunomodulation / Q000276:immunology; D020521:Stroke / Q000276:immunology*; D015533:Transcriptional Activation
D016328:NF-kappa B