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Endocrine, Metabolic & Immune Disorders - Drug Targets

Editor-in-Chief

ISSN (Print): 1871-5303
ISSN (Online): 2212-3873

NF-κ B and Rheumatic Diseases

Author(s): Takashi Okamoto

Volume 6, Issue 4, 2006

Page: [359 - 372] Pages: 14

DOI: 10.2174/187153006779025685

Price: $65

Abstract

NF-κB is an inducible transcription factor that is controlled by the signal activation cascades. NF-κB controls a number of genes involved in immuno-inflammatory responses, cell cycle progression, inhibition of apoptosis, and cell adhesion, thus promoting chronic inflammatory responses. In fact, NF-κB is constitutively activated in some rheumatic conditions such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Interestingly, a number of anti-RA compounds have been shown to exhibit anti-NF-κB activities. In addition, NF-κB activation has been linked to carcinogenesis and its constitutive activation has been demonstrated in some cancers and leukemias. These findings have substantiated the long-standing proposal of the link among chronic inflammation, autoimmunity, and carcinogenesis by molecular terms. In this review, I have attempted to overview the pathologic involvement of NF-κB in rheumatic diseases and discuss the feasibility of a therapeutic strategy with NF-κB and its signaling cascade as novel molecular targets.

Keywords: NF-κ B, signal transduction, IKK, transcription, apoptosis, inflammation, autoimmunity, rheumatoid arthritis, systemic lupus erythematosus, inhibitors


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