| 骨性关节炎发病机制的研究进展 |
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投稿时间：2020-03-20
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| 作者 | Author | 单位 | Address | E-Mail |
| 唐金烁 |
TANG Jin-shuo |
吉林大学中日联谊医院骨关节科, 吉林 长春 130031 |
Department of Orthopaedics and Joint, China-Japan Union Hospital of Jilin University, Changchun 130031, Jilin, China |
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| 周忠圣 |
ZHOU Zhong-sheng |
吉林大学中日联谊医院骨关节科, 吉林 长春 130031 |
Department of Orthopaedics and Joint, China-Japan Union Hospital of Jilin University, Changchun 130031, Jilin, China |
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| 肖建林 |
XIAO Jian-lin |
吉林大学中日联谊医院骨关节科, 吉林 长春 130031 |
Department of Orthopaedics and Joint, China-Japan Union Hospital of Jilin University, Changchun 130031, Jilin, China |
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| 高忠礼 |
GAO Zhong-li |
吉林大学中日联谊医院骨关节科, 吉林 长春 130031 |
Department of Orthopaedics and Joint, China-Japan Union Hospital of Jilin University, Changchun 130031, Jilin, China |
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| 左建林 |
ZUO Jian-lin |
吉林大学中日联谊医院骨关节科, 吉林 长春 130031 |
Department of Orthopaedics and Joint, China-Japan Union Hospital of Jilin University, Changchun 130031, Jilin, China |
zuojl@jlu.edu.cn |
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| 期刊信息：《中国骨伤》2021年，第34卷，第10期，第985-990页 |
| DOI：10.12200/j.issn.1003-0034.2021.10.018 |
| 基金项目: |
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| 中文摘要:骨性关节炎（osteoarthritis，OA）是最常见的关节疾病之一。随着中国社会跨入老龄化时代，OA发病率逐年升高，对于其发病机制的研究也受到研究人员不断重视。研究发现，以白细胞介素1β（interle ukin-1β，IL-1β）和肿瘤坏死因子α（tumor necrosis factor-α，TNF-α）为主的炎症细胞因子是组建起OA炎症网络的罪魁祸首。并且发现以基质金属蛋白酶（matrix metalloproteinase，MMPs）和含血小板反应蛋白基序的解聚素样金属蛋白酶（a disintegrin and metalloproteinase with thrombospondin motifs，ADAMTS）为主的蛋白酶过度表达，是造成OA软骨缺如的直接原因。此外，基质细胞衍生因子-1（stromal cell derived factor-1，SDF-1）和Wnt等信号通路，软骨细胞衰老与衰老相关分泌表型（senescence-associated secretory phenotype，SASP），软骨细胞凋亡与自噬，雌激素等均在OA发病中发挥了重要作用。本文广泛查阅了近几年与OA发病机制有关的研究文献，从分子层次与细胞层次两方面对OA发病机制进行了系统阐述。并且于文末谈论预测了未来OA临床诊疗中的一些潜在方向。 |
| 【关键词】骨关节炎 发病机制 综述文献 |
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| Research progression in the pathogenesis of osteoarthritis |
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| ABSTRACT Osteoarthritis(OA) is one of the most common joint diseases. As Chinese society enters the age of aging,the incidence of OA has been soar year by year,and research on its pathogenesis has been continuously valued by researchers. Studies have found that inflammatory cytokines,mainly interleukin-1β(IL-1β) and tumor necrosis factor-α (TNF-α),were responsible for the construction of OA inflammatory networks. It was also found that the overexpression of proteases,mainly matrix metalloproteinases(MMPs) and a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS),was the direct cause of OA cartilage deficiency. What's more,signaling pathways such as stromal cell derived factor-1(SDF-1) and Wnt,chondrocytic senescence and the senescence-associated secretory phenotype (SASP),chondrocyte apoptosis and autophagy,and estrogen all play significant roles in OA pathogenesis. This paper extensively reviews the research literature relevant to the pathogenesis of OA in recent years,and systematically expounds the pathogenesis of OA from two aspects:molecular level and cell level. At the end of the paper,we discussed and predicted some potential directions in the future clinical diagnosis and treatment of OA. |
| KEY WORDS Osteoarthritis Pathogenesis Review literature |
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| 引用本文，请按以下格式著录参考文献： |
| 中文格式: | 唐金烁,周忠圣,肖建林,高忠礼,左建林.骨性关节炎发病机制的研究进展[J].中国骨伤,2021,34(10):985~990 |
| 英文格式: | TANG Jin-shuo,ZHOU Zhong-sheng,XIAO Jian-lin,GAO Zhong-li,ZUO Jian-lin.Research progression in the pathogenesis of osteoarthritis[J].zhongguo gu shang / China J Orthop Trauma ,2021,34(10):985~990 |
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