NF-κB signaling in cerebral ischemia

D. A. Ridder, M. Schwaninger*

*Corresponding author for this work
220 Citations (Scopus)


The transcription factor NF-κB is a key regulator of hundreds of genes involved in cell survival and inflammation. There is ample evidence that NF-κB is activated in cerebral ischemia, mainly in neurons. Despite its well known role as an antiapoptotic factor, in cerebral ischemia NF-κB contributes to neuronal cell death, at least if the ischemia is severe enough to lead to irreversible brain damage. In contrast, NF-κB also seems to be responsible for the preconditioning effect of a transient and sublethal ischemia, perhaps by dampening its own subsequent full activation. Among the five NF-κB subunits, RelA and p50 are responsible for the detrimental effect in cerebral ischemia. Activation of NF-κB signaling is mediated by the upstream kinase inhibitor of kappaB kinase and is triggered by hypoxia, reactive oxygen species, and several inflammatory mediators. Interestingly, the complex NF-κB signaling pathway provides drug targets at several levels. Modulation of NF-κB signaling has the potential to interrupt multiple inflammatory and apoptotic mechanisms through one specific molecular target.

Original languageEnglish
Issue number3
Pages (from-to)995-1006
Number of pages12
Publication statusPublished - 06.02.2009

Research Areas and Centers

  • Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)


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