Basic & Clinical Medicine ›› 2026, Vol. 46 ›› Issue (9): 1293-1297.doi: 10.16352/j.issn.1001-6325.2026.09.1293

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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

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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