The New York University School of Medicine, New York, NY, USA.
Vanderbilt University Medical Center, Nashville, TN, USA.
Nat Rev Rheumatol. 2020 Mar;16(3):145-154. doi: 10.1038/s41584-020-0373-9. Epub 2020 Feb 17.
Despite the introduction of numerous biologic agents for the treatment of rheumatoid arthritis (RA) and other forms of inflammatory arthritis, low-dose methotrexate therapy remains the gold standard in RA therapy. Methotrexate is generally the first-line drug for the treatment of RA, psoriatic arthritis and other forms of inflammatory arthritis, and it enhances the effect of most biologic agents in RA. Understanding the mechanism of action of methotrexate could be instructive in the appropriate use of the drug and in the design of new regimens for the treatment of RA. Although methotrexate is one of the first examples of intelligent drug design, multiple mechanisms potentially contribute to the anti-inflammatory actions of methotrexate, including the inhibition of purine and pyrimidine synthesis, transmethylation reactions, translocation of nuclear factor-κB (NF-κB) to the nucleus, signalling via the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway and nitric oxide production, as well as the promotion of adenosine release and expression of certain long non-coding RNAs.
尽管已经有许多生物制剂被用于治疗类风湿关节炎(RA)和其他形式的炎性关节炎,但低剂量甲氨蝶呤治疗仍然是 RA 治疗的金标准。甲氨蝶呤通常是治疗 RA、银屑病关节炎和其他形式的炎性关节炎的一线药物,它可以增强 RA 中大多数生物制剂的疗效。了解甲氨蝶呤的作用机制对于正确使用该药物以及设计新的 RA 治疗方案可能具有指导意义。虽然甲氨蝶呤是智能药物设计的首批范例之一,但多种机制可能有助于甲氨蝶呤的抗炎作用,包括嘌呤和嘧啶合成的抑制、转甲基反应、核因子-κB(NF-κB)向核内的易位、通过 Janus 激酶(JAK)-信号转导和转录激活物(STAT)途径的信号传递以及一氧化氮的产生,以及促进腺苷的释放和某些长非编码 RNA 的表达。