中文摘要：

类风湿关节炎（rheumatoid arthritis,RA）是一种系统性自身免疫性疾病,病理特征为异常的滑膜增生伴血管翳形成、软骨和骨的侵蚀破坏,最终导致关节畸形。目前RA确切发病机制未明,环境和遗传因素相互作用共同促进了RA的发病。低氧微环境是RA重要的病理特点,炎症滑膜组织的高代谢需求和滑膜的快速增生共同导致了RA关节内低氧状态。

英文摘要：

Rheumatoid arthritis（ RA） is a destructive chronic autoimmune disease characterized by synovium inflammation,cartilage destruction,bone erosion and the presence of autoantibodies. Hypoxia is a prominent micro-environmental feature in a range of disorders including RA. A combination of increased oxygen consumptionby inflamed resident cells and infiltrating immune cells along with a disrupted blood supply due to vascular dysfunction contribute to tissue hypoxia in RA. Hypoxia in turn regulates a number of key signaling pathways that help adaptation. The primary signaling pathway activated by hypoxia is the hypoxia-inducible factor（ HIF） pathway. It has been shown that HIFs are highly expressed in the synovium of RA. HIFs mediate the pathogenesis of RA through inducing inflammation,angiogenesis,cell migration,and cartilage destruction,and inhibiting the apoptosis of synovial cells and inflammatory cells. HIF expressed in RA can be regulated in both oxygen-dependent and independent fashions,like inflammatory cytokines,leading to the aggravation of this disease. Considering the vital role of HIF in the pathogenesis of RA,we reviewed the new advances about hypoxia and RA. In this review,we firstly discussed the hypoxia-inducible factor and its regulation,and then,the pathologic role of hypoxia in RA,mainly elucidating the role of hypoxia in synovitis and cartilage destruction and immune cells. Finally,we provided evidence about the potential therapeutic target for treating RA.