细胞衰老在骨关节炎发病机制中的研究进展  

Research progress of cellular senescence in the pathogenesis of osteoarthritis

作　　者：谢锦伟[1,2,3] 鲁凌云 余希杰[2,5] XIE Jinwei;LU Lingyun;YU Xijie(Department of Orthopaedics,West China Hospital,Sichuan University,Chengdu Sichuan,610041,P.R.China;Laboratory of Endocrinology and Metabolism,West China Hospital,Sichuan University,Chengdu Sichuan,610041,P.R.China;National Clinical Research Center for Geriatrics,West China Hospital,Sichuan University,Chengdu Sichuan,610041,P.R.China;Department of Integrated Traditional Chinese and Western Medicine,West China Hospital,Sichuan University,Chengdu Sichuan,610041,P.R.China;Department of Endocrinology and Metabolism,West China Hospital,Sichuan University,Chengdu Sichuan,610041,P.R.China)

机构地区：[1]四川大学华西医院骨科,成都610041 [2]四川大学华西医院内分泌与代谢病研究室,成都610041 [3]四川大学华西医院国家老年疾病临床医学研究中心,成都610041 [4]四川大学华西医院中西医结合科,成都610041 [5]四川大学华西医院内分泌代谢科,成都610041

出　　处：《中国修复重建外科杂志》2021年第4期519-526,共8页Chinese Journal of Reparative and Reconstructive Surgery

基　　金：国家自然科学基金资助项目(81902246);四川省科技厅重点研发专项(2020YFS0142);四川大学华西医院博士后研发基金(2018HXBH073);国家老年疾病临床研究中心项目(Z2018B11)。

摘　　要：目的综述细胞衰老在骨关节炎(osteoarthritis,OA)发生、发展中的病理作用及潜在治疗靶点。方法查阅国内外相关文献,对软骨细胞衰老、滑膜细胞衰老、MSCs衰老在OA中的作用及软骨细胞衰老发生的生物学机制和进展进行总结。结果现有证据已基本明确软骨细胞衰老、MSCs衰老与软骨修复异常及OA的发生、发展存在一定因果关系,而滑膜细胞衰老,特别是滑膜巨噬细胞衰老在OA中的作用尚不明确。转录因子、表观遗传是调控衰老上游通路的主要机制,细胞间的信号交流可促进健康细胞出现衰老表型。定向清除衰老细胞和促进MSCs年轻化可有效延缓OA的进展。结论细胞衰老是OA发生、发展中的重要生物学现象及潜在治疗靶点,深入研究其生物学机制有助于OA的早期防治。Objective To review the pathological effects of cellular senescence in the occurrence and development of osteoarthritis(OA) and potential therapeutic targets. Methods The role of chondrocyte senescence,synovial cell senescence, mesenchymal stem cells senescence in OA, and the biological mechanism and progress of chondrocyte senescence were summarized by consulting relevant domestic and abroad literature. Results The existing evidence has basically made clear that chondrocyte senescence, mesenchymal stem cells senescence, and cartilage repair abnormalities, and the occurrence and development of OA have a certain causal relationship, and the role of the senescence of synovial cells, especially synovial macrophages in OA is still unclear. Transcription factors and epigenetics are the main mechanisms that regulate the upstream pathways of cellular senescence. Signal communication between cells can promote the appearance of senescent phenotypes in healthy cells. Targeted elimination of senescent cells and promotion of mesenchymal stem cells rejuvenation can effectively delay the progress of OA. Conclusion Cellular senescence is an important biological phenomenon and potential therapeutic target in the occurrence and development of OA. In-depth study of its biological mechanism is helpful to the early prevention and treatment of OA.

关 键 词：骨关节炎 细胞衰老 软骨细胞 细胞年轻化 

分 类 号：R684.3[医药卫生—骨科学]