基础医学与临床 ›› 2026, Vol. 46 ›› Issue (9): 1293-1297.doi: 10.16352/j.issn.1001-6325.2026.09.1293

• 短篇综述 • 上一篇    下一篇

双硫死亡在骨关节炎中的作用

李娜1, 马立凯2, 张君蕾2, 丁宁2, 马丽3*   

  1. 陕西中医药大学 1.基础学院;2.中医学院;3.动物医学院;陕西 咸阳 712046
  • 收稿日期:2026-04-28 修回日期:2026-05-28 出版日期:2026-09-05 发布日期:2026-08-18
  • 通讯作者: *malisxzyydx@163.com
  • 基金资助:
    秦创原中医药产业创新聚集区项目(L2024-QCY-ZYYJJQ-X08);陕西省教育厅科学研究项目(25JK0416);陕西省自然科学基础研究计划(2023-JC-QN-0900);陕西中医药大学大学生创新创业项目(S202410716049,S202510716070)

Role of disulfidptosis in osteoarthritis

LI Na1, MA Likai2, ZHANG Junlei2, DING Ning2, MA Li3*   

  1. 1. College of Basic Medicine; 2. College of Traditional Chinese Medicine; 3. College of Veterinary Medicine, Shaanxi University of Chinese Medicine, Xianyang 712046, China
  • Received:2026-04-28 Revised:2026-05-28 Online:2026-09-05 Published:2026-08-18
  • Contact: *malisxzyydx@163.com

摘要: 双硫死亡是一种新型的程序性细胞死亡方式。其核心机制表现为:在胱氨酸转运体溶质载体家族7成员11(SLC7A11)高表达的细胞中,葡萄糖缺乏导致烟酰胺腺嘌呤二核苷酸磷酸(NADPH)耗竭,胱氨酸还原受阻并异常积聚,诱发二硫应激,进而攻击肌动蛋白,经Rac1-WRC通路放大后引起细胞骨架不可逆崩溃。双硫死亡相关基因表达失调通过诱导软骨细胞死亡,调控软骨细胞-免疫细胞间信号交互促进骨关节炎的炎症微环境,决定骨关节炎的分子异质性等方式影响骨关节炎的疾病进展。针对SLC3A2等关键分子的干预可在实验模型中缓解病理改变,提示靶向双硫死亡具有治疗潜力。

关键词: 双硫死亡, 骨关节炎, 软骨细胞, 炎症反应

Abstract: Disulfidptosis is a newly fond form of program cell death. Its core mechanism is characterized by cystine transporter solute carrier family 7 member 11(SLC7A11) expression, glucose deprivation leading to nicotinamide adenine dinucleotide phosphate(NADPH) depletion, impaired reduction and subsequent abnormal accumulation of cystine which triggers disulfide stress. This stress then attacks actin, and the damage is amplified through the Rac1-WRC pathway causing irreversible cytoskeleton collapse. Dysregulated expression of disulfidptosis-related genes influences the progression of osteoarthritis through multiple mechanisms, including inducing chondrocyte death, modulating chondrocyte-immune cell crosstalk to promote the inflammatory microenvironment of osteoarthritis, and determining the molecular heterogeneity of osteoarthritis. Targeting key molecules like SLC3A2 alleviate pathological changes in experimental models, indicating the therapeutic potential of targeting disulfidptosis.

Key words: disulfidptosis, osteoarthritis, chondrocyte, inflammation

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