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T-2 toxin exacerbates chondrocyte extracellular matrix degradation potentially through YAP/NLRP3/GSDMD-mediated

Haonan Li1, Zhifeng Xing1, Hexuan Dong2

  • 1Institute for Kashin-Beck Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin 150081, Heilongjiang, China.; National Healthy Commission and Education Bureau of Heilongjiang Province, Key Laboratory of Etiology and Epidemiology, Harbin Medical University (23618504), Heilongjiang Provincial Laboratory of Trace Element and Human Health, Harbin Medical University, Harbin 150081, China.

International Immunopharmacology
|November 23, 2025
PubMed

Insights

T-2 toxin causes cartilage damage in Kashin-Beck disease by activating the YAP/NLRP3/GSDMD pathway. Inhibiting YAP protects against this damage, highlighting a potential therapeutic target for this endemic osteoarthropathy.

Area of Science:

  • Biochemistry
  • Pathology
  • Molecular Biology

Background:

  • Kashin-Beck disease (KBD) is an endemic osteoarthropathy linked to T-2 toxin.
  • The pathogenic mechanisms of T-2 toxin-induced cartilage injury require further elucidation.

Purpose of the Study:

  • To investigate the role of the YAP/NLRP3/GSDMD signaling pathway in T-2 toxin-induced cartilage injury.
  • To identify potential therapeutic targets for KBD.

Main Methods:

  • KEGG pathway enrichment analysis of KBD-associated genes from PubMed.
  • Analysis of serum levels of IL-1β, IL-18, and LDH in KBD patients.
  • In vivo and in vitro experiments using T-2 toxin models, YAP inhibition (verteporfin), and YAP overexpression.

Main Results:

  • T-2 toxin inhibited Hippo/YAP signaling, promoted YAP nuclear translocation, and activated NLRP3/GSDMD-mediated pyroptosis and extracellular matrix (ECM) degradation.
  • Elevated serum IL-1β, IL-18, and LDH were observed in KBD patients.
  • YAP inhibition alleviated pyroptosis and ECM degradation, while YAP overexpression exacerbated these effects.

Conclusions:

  • YAP activation mediates T-2 toxin-induced chondrocyte pyroptosis and ECM degradation via the NLRP3/GSDMD pathway.
  • The YAP/NLRP3/GSDMD pathway represents a key mechanism in KBD pathogenesis and a potential therapeutic target.
Keywords:
Cartilage injuryKashin-Beck diseasePyroptosisT-2 toxinYes-associated protein

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