内质网应激在骨关节炎中作用的研究进展  

Research progress on the role of endoplasmic reticulum stress in osteoarthritis

作　　者：金涛[1,2] 杨青山 吴树金[3] 朱晓燕 史宇悰 牛建雄 刘林 JIN Tao;YANG Qingshan;WU Shujin;ZHU Xiaoyan;SHI Yucong;NIU Jianxiong;LIU Lin(The First Clinical College,Gansu University of Traditional Chinese Medicine,Lanzhou 730000;Department of Orthopedics,Gansu Provincial People's Hospital,Lanzhou 730000;School of Pharmacy,Lanzhou University,Lanzhou 730000,China)

机构地区：[1]甘肃中医药大学第一临床医学院,甘肃兰州730000 [2]甘肃省人民医院骨科,甘肃兰州730000 [3]兰州大学药学院,甘肃兰州730000

出　　处：《基础医学与临床》2023年第3期476-480,共5页Basic and Clinical Medicine

基　　金：国家自然科学基金(8176090197)。

摘　　要：骨关节炎是一种常见的关节退变性疾病,软骨细胞凋亡是其主要的病理生理改变,而内质网应激(ER stress)在其中发挥了不可忽视的作用。为了限制内质网应激带来的不利影响,细胞会激活未折叠蛋白质应答(UPR)。然而当内质网应激持续存在超过UPR所能承受的最大限度时,细胞会通过UPR的3条通路引发内质网功能障碍从而导致软骨细胞凋亡。Osteoarthritis is a common degenerative disease in which endoplasmic reticulum stress(ER stress) plays an important role in the pathogenesis of chondrocyte apoptosis.To limit the adverse effects of endoplasmic reticulum stress,cells activate the unfolded protein response(UPR).However,when endoplasmic reticulum stress persists beyond the maximum tolerance of UPR,cells may trigger endoplasmic reticulum dysfunction through three pathways of UPR leading to chondrocyte apoptosis.

关 键 词：骨关节炎 软骨细胞凋亡 内质网应激 未折叠蛋白质应答 

分 类 号：R684.3[医药卫生—骨科学]