Journal
EXPERT OPINION ON THERAPEUTIC TARGETS
Volume 23, Issue 7, Pages 607-618Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/14728222.2019.1617274
Keywords
Autoimmunity; FK866; IL1 beta; IL6; inflammation; NAMPT; RA; RASF; TLRs; Visfatin
Categories
Funding
- Fondo de Investigacion Sanitaria - the Instituto de Salud Carlos III (ISCIII)
- Fondo Europeo de Desarrollo Regional FEDER [PI16/01870, CP15/00007, PI14/00016, PI17/00409]
- ISCIII
- Servizo Galego de Saude SERGAS through a Miguel Servet programme
- RETICS program from ISCIII [RD16/0012/0014]
- European Union, MSCA- Q4 RISE-H2020 program [734899]
- Mutua Madrilena Fundation (MMA 2018)
- Muta Madrilena Fundation
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Introduction: The rising prevalence of musculoskeletal pathologies in developed countries has caused a dramatic impact on social welfare. Amidst these musculoskeletal pathologies is Rheumatoid arthritis (RA), a chronic systemic autoimmune disease that mostly affects the synovium. RA metabolic-associated alterations, including distorted adipokine production, enhance RA inflammatory environment. Among the altered adipokines, visfatin is particularly involved in RA inflammation and catabolism and stands out as an essential enzyme linked to critical cell features. Areas covered: We discuss the potential mechanism supporting the contribution of visfatin to RA and the association between RA and obesity. We discuss the repurposing of cancer-tested drugs to inhibit visfatin in the context of RA. Additionally, we address the possibility of combining these drugs with current RA therapy. Finally, we explore the future of visfatin as an RA biomarker or therapeutic target. Expert opinion: Inhibition of visfatin has become an interesting therapeutic approach for RA pathology. Such a feat has already been attained in oncology using small molecule inhibitors, which suggest that a similar course of action would be worth pursuing in the RA context. Visfatin will become an important biomarker and therapeutic target for RA.
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