Publisher: Bentham Science Publishers
E-ISSN: 2212-3873|6|4|359-372
ISSN: 1871-5303
Source: Endocrine, Metabolic & Immune Disorders-Drug Targets (Formerly Current Drug Targets - Immune, Endocrine & Metabolic Disorders), Vol.6, Iss.4, 2006-12, pp. : 359-372
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Abstract
NF-&kgr;B is an inducible transcription factor that is controlled by the signal activation cascades. NF-&kgr;B 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-&kgr;B 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-&kgr;B activities. In addition, NF-&kgr;B 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-&kgr;B in rheumatic diseases and discuss the feasibility of a therapeutic strategy with NF-&kgr;B and its signaling cascade as novel molecular targets.
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