【摘要】 类风湿关节炎(rheumatoid arthritis, RA)是常见的自身免疫性疾病，以滑膜炎症、骨质破坏和血管翳形成为主要病理特征。其中，葡萄糖代谢失常显著促进了RA的致病行为，特别是己糖激酶2(Hexokinase 2,HK2)可以通过介导糖酵解代谢促进炎症反应、抑制细胞凋亡、促进细胞自噬、诱导线粒体氧化应激，并在免疫调节、骨质破坏和适应缺氧中发挥关键作用，故HK2的异常调节可能参与RA发病的分子机制，并可能成为RA治疗极具吸引力的一个选择性代谢靶点。基于此，笔者系统综述了HK2在RA发病机制中的最新文献，以期为RA的发病机制及治疗途径提供新的参考依据。更多还原

【Abstract】 Rheumatoid arthritis(RA) is a common autoimmune disease characterized by synovitis, bone destruction, and pannus formation. Among them, abnormal glucose metabolism significantly promotes the pathogenic behavior of RA. Especially, hexokinase 2(HK2) promotes inflammation, inhibits apoptosis, promotes autophagy, induces mitochondrial oxidative stress by mediating glycolysis metabolism, and plays a key role in immune regulation, bone destruction, and adaptation to hypoxia. Therefore, the abnormal regulation of HK2 may be involved in the molecular mechanism of RA and may become a very attractive alternative metabolic target for RA therapy. Based on this, this paper systematically reviews the latest literature of HK2 in the pathogenesis of RA, in order to provide new reference basis for the pathogenesis and treatment of RA.更多还原