中国组织工程研究

中国组织工程研究 ›› 2026, Vol. 30 ›› Issue (24): 6282-6288.doi: 10.12307/2026.213

• 组织构建综述 tissue construction review • 上一篇    下一篇

软骨细胞铁死亡在骨关节炎发病中的作用

苏介茂1，2，齐岩松2，孔柯瑜3，翟赞京3，徐永胜1，2   

  1. 1内蒙古医科大学内蒙古临床医学院，内蒙古自治区呼和浩特市   010017；2内蒙古自治区人民医院骨科中心(运动医学中心)，内蒙古自治区呼和浩特市   010017；3上海交通大学医学院附属第九人民医院骨科，上海市   200011
  • 收稿日期:2025-08-04 修回日期:2025-09-10 出版日期:2026-08-28 发布日期:2026-02-03
  • 通讯作者: 徐永胜，主任医师，博士生导师，内蒙古医科大学内蒙古临床医学院，内蒙古自治区呼和浩特市 010017；内蒙古自治区人民医院骨科中心(运动医学中心)，内蒙古自治区呼和浩特市 010017 通讯作者：齐岩松，副主任医师，副研究员，内蒙古自治区人民医院骨科中心(运动医学中心)，内蒙古自治区呼和浩特市 010017
  • 作者简介:苏介茂，男，1999年生，内蒙古自治区巴彦淖尔市人，汉族，在读硕士，主要从事运动医学基础与临床研究。
  • 基金资助:
    内蒙古自治区自然科学基金项目(2024ZD32)，项目负责人：徐永胜；内蒙古自治区自然科学基金项目(2024LHMS08015)，项目负责人：齐岩松；内蒙古自治区首府地区公立医院高水平临床专科建设科技项目(2024SGGZ015)，项目负责人：徐永胜

Role of chondrocyte ferroptosis in the pathogenesis of osteoarthritis

Su Jiemao1, 2, Qi Yansong2, Kong Keyu3, Zhai Zanjing3, Xu Yongsheng1, 2   

  1. 1Inner Mongolia Clincal Medical College, Inner Mongolia Medical University, Hohhot 010017, Inner Mongolia Autonomous Region, China; 2Orthopedic Center (Sport Medicine Center), Inner Mongolia People’s Hospital, Hohhot 010017, Inner Mongolia Autonomous Region, China; 3Department of Orthopaedic Surgery, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200011, China
  • Received:2025-08-04 Revised:2025-09-10 Online:2026-08-28 Published:2026-02-03
  • Contact: Xu Yongsheng, Chief physician, Doctoral supervisor, Inner Mongolia Clincal Medical College, Inner Mongolia Medical University, Hohhot 010017, Inner Mongolia Autonomous Region, China; Orthopedic Center (Sport Medicine Center), Inner Mongolia People’s Hospital, Hohhot 010017, Inner Mongolia Autonomous Region, China Co-corresponding author: Qi Yansong, Associate chief physician, Associate researcher, Orthopedic Center (Sport Medicine Center), Inner Mongolia People's Hospital, Hohhot 010017, Inner Mongolia Autonomous Region, China
  • About author:Su Jiemiao, MS candidate, Inner Mongolia Clincal Medical College, Inner Mongolia Medical University, Hohhot 010017, Inner Mongolia Autonomous Region, China; Orthopedic Center (Sport Medicine Center), Inner Mongolia People’s Hospital, Hohhot 010017, Inner Mongolia Autonomous Region, China
  • Supported by:
    Inner Mongolia Autonomous Region Natural Science Foundation, No. 2024ZD32 (to XYS); Inner Mongolia Autonomous Region Natural Science Foundation, No. 2024LHMS08015 (to QYS); Science and Technology Project for the Construction of High-Level Clinical Specialties in Public Hospitals in the Capital Region of Inner Mongolia Autonomous Region, No. 2024SGGZ015 (to XYS)

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摘要：



文题释义：
铁死亡：是一种由铁离子过载引发的程序性细胞死亡方式。铁死亡的特征是细胞内铁离子浓度异常升高，导致活性氧的产生，进而引发脂质过氧化反应，破坏细胞膜结构，最终导致细胞死亡。与传统的细胞死亡方式如凋亡、坏死不同，铁死亡不涉及细胞核的解体或DNA损伤，而是通过脂质过氧化和膜结构损伤来执行。
骨关节炎：是一种以关节软骨退化为主要特征的慢性炎症性疾病，发病机制复杂，病理特点为关节软骨变性破坏、软骨下骨硬化或囊性变、关节边缘骨质增生、滑膜病变、关节囊挛缩、韧带松弛或挛缩、肌肉萎缩无力等。

背景：铁死亡作为一种程序性细胞死亡，依赖铁过载所引发的脂质过氧化反应导致软骨细胞死亡，从而加剧关节退变。
目的：总结软骨细胞铁死亡在骨关节炎进展中的分子机制以及针对这一机制的干预策略。
方法：检索中国知网、PubMed、Web of Science数据库，中文检索词为“软骨，铁死亡，核因子E2相关因子2，沉默信息调节因子，PTEN诱导的推定激酶1，基质细胞衍生因子1，纳米颗粒，线粒体自噬，水凝胶”等，英文检索词为“cartilage，ferroptosis，Nrf2，NF-E2-related factor 2，SIRT，Sirtuin，PINK1，PTEN induced putative kinase 1，stromal cell-derived factor 1，SDF1，nanoparticle，mitophagy，hydrogel”等，根据入选标准，最终纳入69篇文献进行综述。
结果与结论：铁死亡的发生机制涉及铁沉积、脂质过氧化、氨基酸代谢异常，其中活性氧累积和脂质过氧化是产生铁死亡信号的必要条件。在骨关节炎中，软骨细胞铁死亡是导致软骨退变的关键病理机制之一。目前针对软骨细胞铁死亡机制及其相关材料的研究主要聚焦于抗氧化途径，多项研究尝试通过构建具有抗氧化性能或调控金属离子分布的材料，来减缓骨关节炎所致的软骨损伤并改善疾病进程；此外，研制通过其他途径干扰铁死亡的材料也是目前研究骨关节炎治疗的重点。然而，这些研究成果仅在细胞和动物实验中产生有效的治疗作用，尚未进行临床研究，未来的研究需进一步探索铁死亡相关信号网络及材料与生物界面之间的相互作用，开发更高效、安全的治疗策略。
https://orcid.org/0009-0006-7790-5010 (苏介茂) 


中国组织工程研究杂志出版内容重点：干细胞；骨髓干细胞；造血干细胞；脂肪干细胞；肿瘤干细胞；胚胎干细胞；脐带脐血干细胞；干细胞诱导；干细胞分化；组织工程

关键词: 骨关节炎, 软骨细胞, 铁死亡, 谷胱甘肽过氧化物酶4, 活性氧, 纳米颗粒, 水凝胶

Abstract: BACKGROUND: As a programmed cell death, ferroptosis relies on lipid peroxidation triggered by iron overload, leading to the death of chondrocytes and the exacerbation of joint degeneration. 
OBJECTIVE: To summarize the molecular mechanism of chondrocyte ferroptosis in the progression of osteoarthritis, and intervention strategies for this mechanism. 
METHODS: A literature search was conducted in the CNKI, PubMed, and Web of Science databases. The Chinese and English search terms were “cartilage, ferroptosis, Nrf2, NF-E2-related factor 2, SIRT, Sirtuin, PINK1, PTEN induced putative kinase 1, stromal cell-derived factor 1, SDF1, nanoparticle, mitophagy, hydrogel.” Based on the inclusion criteria, 69 articles were ultimately selected for review.
RESULTS AND CONCLUSION: The mechanism of ferroptosis involves iron accumulation, lipid peroxidation, and abnormal amino acid metabolism, with reactive oxygen species accumulation and lipid peroxidation being essential prerequisites for generating ferroptosis signals. In osteoarthritis, chondrocyte ferroptosis serves as a key pathological mechanism of cartilage degeneration. Current research on chondrocyte ferroptosis mechanisms and related materials primarily focuses on antioxidant pathways. Multiple studies have attempted to mitigate osteoarthritis-induced cartilage damage and improve disease progression by developing materials with antioxidant properties or those that regulate metal ion distribution. Additionally, creating materials that interfere with ferroptosis through alternative pathways represents a current research priority for osteoarthritis treatment. At present, these research results have only produced effective therapeutic effects in cell and animal experiments, and have not been clinically studied. Future studies need to further explore the ferroptosis-related signaling network and the interaction between materials and biological interfaces to develop more efficient and safe treatment strategies.

Key words: osteoarthritis, chondrocyte, ferroptosis, glutathione peroxidase 4, reactive oxygen species, nanoparticle, hydrogel

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