Objective: Analysis and generalization of data related to visfatin involvement in the
pathogenesis of inflammation at various stages of rheumatoid arthritis.
Data Synthesis: Visfatin is an adipocytokine which has also been identified in non-adipose tissues.
It influences directly on the maturation of B cells, which are involved in autoantibody production
and T cell activation. Visfatin can promote inflammation via regulation of pro-inflammatory cytokines
including TNF, IL-1β and IL-6. The concentration of circulating visfatin in rheumatoid arthritis
patients is higher compared to healthy individuals. Several studies suggest that visfatin level is
associated with rheumatoid arthritis activity, and its elevation may precede clinical signs of the relapse.
In murine collagen-induced arthritis, visfatin levels were also found to be elevated both in
inflamed synovial cells and in joint vasculature. Visfatin blockers have been shown to confer fast
and long-term attenuation of pathological processes; however, most of their effects are transient.
Other factors responsible for hyperactivation of the immune system can participate in this process
at a later stage. Treatment of rheumatoid arthritis with a combination of these blockers and inhibitors
of other mediators of inflammation can potentially improve treatment outcomes compared to
current therapeutic strategies. Recent advances in the treatment of experimental arthritis in mice as
well as the application of emerging treatment strategies obtained from oncology for rheumatoid arthritis
management could be a source of novel adipokine-mediated anti-rheumatic drugs.
Conclusion: The ongoing surge of interest in anticytokine therapy makes further study of visfatin
highly relevant as it may serve as a base for innovational RA treatment.