Visfatin and Rheumatoid Arthritis: Pathogenetic Implications and Clinical Utility.

Autor:	Polyakova YV; Research Institute for Clinical and Experimental Rheumatology, Volgograd, Russian Federation., Zavodovsky BV; Research Institute for Clinical and Experimental Rheumatology, Volgograd, Russian Federation., Sivordova LE; Research Institute for Clinical and Experimental Rheumatology, Volgograd, Russian Federation., Akhverdyan YR; Research Institute for Clinical and Experimental Rheumatology, Volgograd, Russian Federation., Zborovskaya IA; Research Institute for Clinical and Experimental Rheumatology, Volgograd, Russian Federation.
Jazyk:	angličtina
Zdroj:	Current rheumatology reviews [Curr Rheumatol Rev] 2020; Vol. 16 (3), pp. 224-239.
DOI:	10.2174/1573397115666190409112621
Abstrakt:	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. (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)
Databáze:	MEDLINE
Externí odkaz:	Zobrazit plný text záznamu