自噬在骨关节炎中的作用机制及研究进展

doi:10.3877/cma.j.issn.1674-134X.2026.03.010

骨关节炎（OA）是临床上最常见的慢性退行性关节疾病，其核心特征包括关节软骨进行性破坏、软骨下骨异常重塑和滑膜炎症，迄今仍缺乏根治性治疗手段。自噬作为维持细胞内稳态的核心降解机制，其功能失调是驱动OA发生发展的重要因素，且在OA进程中呈现出动态阶段性双重调控特性，活性异常会直接影响软骨细胞的存活状态。本文系统梳理了OA中自噬的多层级交互调控网络，重点阐述了以哺乳动物雷帕霉素靶蛋白（mTOR）为核心的信号通路、叉头框O（FoxO）/沉默信息调节因子2同源物（SIRT）/缺氧诱导因子（HIF）等关键分子节点，以及非编码RNA的表观调控作用与外泌体介导的细胞间通讯机制，为精准靶向自噬治疗OA提供系统性的理论依据。

关键词: 骨关节炎, 软骨细胞, 自噬, 信号传导

Osteoarthritis (OA) is the most common chronic degenerative joint disease in clinical practice. Its core characteristics include progressive degradation of articular cartilage, abnormal remodeling of subchondral bone, and synovial inflammation; to date, there remains no curative treatment. Autophagy, as a core degradation mechanism for maintaining intracellular homeostasis, plays a crucial role in the pathogenesis and progression of OA due to its functional dysregulation. It exhibits dynamic, phasic, and bidirectional regulatory characteristics throughout the OA process, and abnormalities in its activity directly affect the survival status of chondrocytes. This article systematically reviewed the multilevel interactive regulatory network of autophagy in OA, focusing on the mTOR-centered signaling pathway, key molecular nodes such as forkhead box O (FoxO)/silent mating type information regulation 2 homolog (SIRT)/hypoxia inducible factor (HIF), as well as the epigenetic regulatory roles of non-coding RNAs and exosome-mediated intercellular communication mechanisms, thereby providing a systematic theoretical basis for precision-targeted autophagy-based therapies for OA.

Key words: osteoarthritis, chondrocyte, autophagy, signaling pathway

图1 OA软骨细胞自噬信号通路及关键分子机制图

Figure 1 Schematic diagram of autophagy signaling pathways and key molecular mechanisms in chondrocytes with osteoarthritis

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Mechanism of autophagy in osteoarthritis and its research progress

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Mechanism of autophagy in osteoarthritis and its research progress