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• W2026385570 abstract "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].In this issue of Cardiovascular Research, Onai et al. [6] report that a novel inhibitor of the activation of NF-κB (IMD-0354) reduces myocardial infarct size in the rat. Using an NF-κB–IKKβ reporter assay in human hepatoma cells transfected with a constitutively active mutant of IKKβ, the authors report that concentrations of less than 1 … *Tel.: +44-207-9826199l; fax: +44-207-2511685. Email address: c.thiemermann{at}qmul.ac.uk" @default.
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• W2026385570 date "2004-07-01" @default.
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• W2026385570 title "Inhibition of the activation of nuclear factor kappa B to reduce myocardial reperfusion injury and infarct size" @default.
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• W2026385570 doi "https://doi.org/10.1016/j.cardiores.2004.04.023" @default.
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