氧化应激在骨关节炎中的研究进展  

Research Progress of Oxidative Stress in Osteoarthritis

作　　者：曹燕[1] 李雪萍[1] CAO Yan;LI Xueping(Department of Rehabilitation Medicine,Nanjing First Hospital/Nanjing Medical University Affiliated Nanjing Hospital,Nanjing 210006,China)

机构地区：[1]南京医科大学附属南京医院南京市第一医院康复医学科,南京210006

出　　处：《医学综述》2021年第19期3779-3784,共6页Medical Recapitulate

基　　金：国家自然科学基金(81772437)。

摘　　要：骨关节炎是与年龄相关的慢性关节疾病,临床表现为关节疼痛、肿胀僵硬以及活动受限等。骨关节炎的发病机制与软骨退变、创伤、代谢等因素有关,其中氧化应激是骨关节炎发生发展的关键因素之一。在软骨细胞中活性氧类的过量积累可引起氧化应激,并通过诱导软骨细胞凋亡、自噬调节失衡、转录后调控等导致软骨细胞损伤和基质降解,促进骨关节炎的进展。其中多种氧化还原相关的信号转导通路(包括核因子κB通路、核因子红系2相关因子2通路、沉默信息调节因子2同源蛋白1通路等)参与骨关节炎的发生发展。进一步研究相关的信号转导靶点,可为骨关节炎的治疗提供新方向。Osteoarthritis is an age-related chronic joint disease,and its clinical manifestations include joint pain,swelling and stiffness,and limited movement.The pathogenesis of osteoarthritis is related to cartilage degeneration,trauma,metabolism and other factors,among which oxidative stress plays a key role in the occurrence and development of osteoarthritis.Excessive accumulation of reactive oxygen species in chondrocytes can cause oxidative stress,and lead to chondrocyte injury and matrix degradation by inducing apoptosis of chondrocytes,imbalance of autophagy regulation,and post-transcriptional regulation etc.,thus promoting the progress of osteoarthritis.Many redox-related signal transduction pathways,including nuclear factorκB pathway,nuclear factor erythroid 2-related factor 2 pathway and silencing information regulator 2 homologous protein 1 pathway,are involved in the the occurrence and development of osteoarthritis.Further research on the specific signal transduction targets can open up a new direction for the treatment of osteoarthritis.

关 键 词：骨关节炎 氧化应激 发病机制 信号转导通路 

分 类 号：R684.3[医药卫生—骨科学] R34[医药卫生—外科学]