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Christoph Thiemermann, Inhibition of the activation of nuclear factor kappa B to reduce myocardial reperfusion injury and infarct size, Cardiovascular Research, Volume 63, Issue 1, July 2004, Pages 8–10, https://doi.org/10.1016/j.cardiores.2004.04.023
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See article by Onai et al. [6] (pages 51–59) in this issue.
Nuclear factor kappa B (NF-κB) is a transcription factor that plays a pivotal role in the induction of genes involved in physiological processes as well as in the response to injury and inflammation. The process leading to the activation of NF-κB requires phosphorylation of an inhibitor of NF-κB (IκB) by IκB kinase (IKK), resulting in degradation of IκB by the 26S proteasome. This allows the translocation of NF-κB from the cytosol to the nucleus, where the heterodimer binds to a response element in the promotor region of specific target genes. Activation of NF-κB induces gene programs leading to the transcription of factors that promote inflammation (i.e. adhesion molecules, cytokines and chemokines) but may also importantly contribute to tissue remodelling, the resolution of inflammation, and transcription of genes whose products have anti-inflammatory effects. Most notably, activation of NF-κB appears to play a significant role in the pathophysiology of endothelial dysfunction, unstable angina pectoris, acute myocardial infarction and heart failure [1–3]. In addition, prevention of the activation of NF-κB has been attributed to at least some of the beneficial effects of certain beta-blockers and statins [4 5].
