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Cardiovascular Research 2004 63(1):8-10; doi:10.1016/j.cardiores.2004.04.023
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Inhibition of the activation of nuclear factor kappa B to reduce myocardial reperfusion injury and infarct size

Christoph Thiemermann*

Centre for Experimental Medicine, Nephrology and Critical Care, William Harvey Research Institute, John-Vane Science Centre, Barts and the Royal London School of Medicine and Dentistry, Charterhouse Square, London EC1M6BQ, UK

*Tel.: +44-207-9826199l; fax: +44-207-2511685. Email address: c.thiemermann@qmul.ac.uk

Received 30 March 2004; revised 21 April 2004; accepted 22 April 2004

The first 10% of the full text of this article appears below.

See article by Onai et al. [6] (pages 51–59) in this issue.

Nuclear factor kappa B (NF-{kappa}B) 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-{kappa}B requires phosphorylation of an inhibitor of NF-{kappa}B (I{kappa}B) by I{kappa}B kinase (IKK), resulting in degradation of I{kappa}B by the 26S proteasome. This allows the translocation of NF-{kappa}B 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-{kappa}B induces gene programs leading to the transcription of factors that promote inflammation (i.e. adhesion molecules, cytokines . . . [Full Text of this Article]


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