Role of nuclear factor κB in synovial inflammation

U Müller-Ladner, RE Gay, S Gay - Current rheumatology reports, 2002 - Springer
U Müller-Ladner, RE Gay, S Gay
Current rheumatology reports, 2002Springer
The evaluation of molecular pathways has revealed novel insights into the pathophysiology
of rheumatoid arthritis in the last several years. Gene transcription factors such as nuclear
factor κB (NFκB) are activated by extracellular signals or cell-to-cell interactions that are
converted into intracellular activation signals through receptor molecules located in the cell
membrane. The number of known genes being translated after NFκB activation is increasing
steadily. These genes includes cytokines, chemokines, growth factors, cellular ligands, and …
Abstract
The evaluation of molecular pathways has revealed novel insights into the pathophysiology of rheumatoid arthritis in the last several years. Gene transcription factors such as nuclear factor κB (NFκB) are activated by extracellular signals or cell-to-cell interactions that are converted into intracellular activation signals through receptor molecules located in the cell membrane. The number of known genes being translated after NFκB activation is increasing steadily. These genes includes cytokines, chemokines, growth factors, cellular ligands, and adhesion molecules. Because many of these genes are part of the pathogenesis of RA, there is considerable interest in the evaluation of the synovium-specific effects of NFκB to unveil its potential for future therapeutic strategies. The goal is to evolve these strategies from the therapies that have a wide spectrum of effects and side effects into rheumatoid arthritis-specific therapies designed to inhibit distinct molecular pathways within the synovium.
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