骨性关节炎中细胞衰老机制的多维解析与研究
Multidimensional analysis and research of cellular senescence mechanism in osteoarthritis
  
DOI:10.3969/j.issn.1006-7108.2026.05.019
中文关键词:  细胞衰老  骨性关节炎  机械应力  炎症  氧化应激
英文关键词:cellular senescence  osteoarthritis  mechanical stress  inflammation  oxidative stress
基金项目:甘肃省中医药科研课题(GZKP-2021-13);陇原青年创新创业人才(2023LQTD08);陇原青年英才项目;甘肃省联合科研基金一般项目(24JRRA899)
作者单位
安杰1 刘涛1* 顾玉彪1 田慧卿2 何志军1 陈文1 李岩1 李金鹏1 李非 1 1.甘肃省中医院,甘肃 兰州 730050 2.甘肃中医药大学,甘肃 兰州 730050 
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中文摘要:
      骨关节炎(OA)是一种严重影响中老年人健康的退行性关节疾病,随着人口老龄化加剧,其发病率持续上升,且缺乏根治手段,深入探究其发病机制意义重大。细胞衰老在 OA 发生发展中占据关键地位,多种因素如机械应力、炎症、氧化应激、自噬失衡等相互作用,驱动关节软骨细胞、滑膜细胞和间充质干细胞衰老,致使关节微环境失衡,加速 OA 进程 。目前,相关研究虽取得一定进展,但多聚焦单一因素,对各因素协同作用机制的系统性研究不足,且在转化为临床治疗策略方面面临诸多挑战。本文系统梳理细胞衰老在 OA 中的特征、机制及作用,剖析多因素交互网络,旨在为揭示 OA 发病机制、开发创新治疗方案提供理论依据与研究方向。
英文摘要:
      Osteoarthritis (OA) is a degenerative joint disease that seriously affects the health of middle-aged and elderly people. With the intensification of population aging, its incidence rate continues to rise, and there is a lack of radical treatment methods. Therefore, it is of great significance to deeply explore its pathogenesis. Cellular senescence plays a crucial role in the occurrence and development of OA. Multiple factors, such as mechanical stress, inflammation, oxidative stress, and autophagic imbalance, interact with each other, driving the senescence of articular chondrocytes, synovial cells, and mesenchymal stem cells. This leads to the imbalance of the joint microenvironment and accelerates the progression of OA. At present, although certain progress has been made in relevant research, most of it focuses on a single factor. There is a lack of systematic research on the synergistic action mechanisms of various factors, and there are many challenges in translating the research results into clinical treatment strategies. This article systematically combs the characteristics, mechanisms, and functions of cellular senescence in OA, and analyzes the interaction network of multiple factors, aiming to provide a theoretical basis and research direction for revealing the pathogenesis of OA and developing innovative treatment options.
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