Rheumatoid arthritis (RA), a multifactorial disease characterized by synovitis, cartilage destruction, bone erosion, and periarticular decalcification, finally results in impairment of joint function. Both genetic and environmental factors are risk factors in the development of RA. Unwanted side effects accompany most of the current treatment strategies, and around 20–40% of patients with RA do not clinically benefit from these treatments. The unmet need for new treatment options for RA has prompted research in the development of novel agents acting through physiologically and pharmacologically relevant targets. Here we discuss in detail three critical pathways, Janus kinase/signal transducer and activator of transcription (JAK/STAT), Th17, and hypoxia-inducible factor (HIF), and their roles as unique therapeutic targets in the field of RA. Some of the less developed but potential targets like nucleotide-binding and oligomerization domain-like receptor containing protein 3 (NLRP3) inflammasome and histone deacetylase 1 (HDAC1) are also discussed.

类风湿关节炎（RA）是一种以滑膜炎，软骨破坏，骨侵蚀和关节周围脱钙为特征的多因素疾病，最终导致关节功能受损。遗传因素和环境因素都是RA发生的危险因素。当前大多数治疗策略均伴随有不良副作用，大约20-40％的RA患者在临床上并未从这些治疗中受益。对RA的新治疗选择的需求未得到满足，促使人们在研究通过生理和药理学相关靶标发挥作用的新型药物方面进行了研究。在这里，我们详细讨论三个关键途径，Janus激酶/信号转导和转录激活因子（JAK / STAT），Th17和缺氧诱导因子（HIF），以及它们在RA领域中作为独特治疗靶标的作用。