Zhang Yiming, Li Jing, Liu Jiane, Gao Yan, Li Kehan, Zhao Xinyu, Liu Yufeng, Wang Daijie, Hu Xiao, Wang Zheng
Department of Genetics and Cell Biology, School of Basic Medicine, Qingdao University, Qingdao, China.
Department of Reproductive Medicine, The Affiliated Hospital of Qingdao University, Qingdao, China.
Cell Prolif. 2025 Mar;58(3):e13779. doi: 10.1111/cpr.13779. Epub 2024 Dec 3.
Osteoarthritis (OA) is a chronic, degenerative joint disease primarily characterised by damage to the articular cartilage, synovitis and persistent pain, and has become one of the most common diseases worldwide. In OA cartilage, various forms of cell death have been identified, including apoptosis, necroptosis and autophagic cell death. Ever-growing observations indicate that ferroptosis, a newly-discovered iron-dependent form of regulated cell death, is detrimental to OA occurrence and progression. In this review, we first analyse the pathogenetic mechanisms of OA by which iron overload, inflammatory response and mechanical stress contribute to ferroptosis. We then discuss how ferroptosis exacerbates OA progression, focusing on its impact on chondrocyte viability, synoviocyte populations and extracellular matrix integrity. Finally, we highlight several potential therapeutic strategies targeting ferroptosis that could be explored for the treatment of OA.
骨关节炎（OA）是一种慢性退行性关节疾病，主要特征为关节软骨损伤、滑膜炎和持续性疼痛，已成为全球最常见的疾病之一。在骨关节炎软骨中，已鉴定出多种形式的细胞死亡，包括凋亡、坏死性凋亡和自噬性细胞死亡。越来越多的观察结果表明，铁死亡是一种新发现的铁依赖性调节性细胞死亡形式，对骨关节炎的发生和发展有害。在本综述中，我们首先分析骨关节炎的发病机制，其中铁过载、炎症反应和机械应激促成铁死亡。然后，我们讨论铁死亡如何加剧骨关节炎的进展，重点关注其对软骨细胞活力、滑膜细胞群体和细胞外基质完整性的影响。最后，我们强调了几种针对铁死亡的潜在治疗策略，可用于探索骨关节炎的治疗方法。
