期刊
SEMINARS IN ARTHRITIS AND RHEUMATISM
卷 51, 期 1, 页码 278-284出版社
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1016/j.semarthrit.2020.10.008
关键词
Cytokines; Inflammation; Janus kinases; Pain; Rheumatoid arthritis; STAT
类别
资金
- Eli Lilly and Company
- National Institute of Health Research of The NIHR Biomedical Research Centre in Musculoskeletal Disease at Oxford University Hospitals NHS Trust
- University of Oxford
Pain in rheumatoid arthritis can be treated by cytokines regulated by the Jak/STAT pathway, which play important roles in regulating inflammation and pain mechanisms.
Pain is a manifestation of rheumatoid arthritis (RA) that is mediated by inflammatory and non-inflammatory mechanisms and negatively affects quality of life. Recent findings from a Phase 3 clinical trial showed that patients with RA who were treated with a Janus kinase 1 (Jak1) and Janus kinase 2 (Jak2) inhibitor achieved significantly greater improvements in pain than those treated with a tumor necrosis factor blocker; both treatments resulted in similar changes in standard clinical measures and markers of inflammation. These findings suggest that Jak1 and Jak2 inhibition may relieve pain in RA caused by inflammatory and non-inflammatory mechanisms and are consistent with the overarching involvement of the Jak-signal transducer and activator of transcription (Jak/STAT) pathway in mediating the action, expression, and regulation of a multitude of pro- and anti-inflammatory cytokines. In this review, we provide an overview of pain in RA, the underlying importance of cytokines regulated directly or indirectly by the Jak/STAT pathway, and therapeutic targeting of the Jak/STAT pathway in RA. As highlighted herein, multiple cytokines directly or indirectly regulated by the Jak/STAT pathway play important roles in mediating various mechanisms underlying pain in RA. Having a better understanding of these mechanisms may help clinicians make treatment decisions that optimize the control of inflammation and pain. (C) 2021 Eli Lilly and Company. Published by Elsevier Inc.
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