Selenium deficiency and T-2 toxin trigger ferroptosis in cartilage from Kashin-Beck diseases

被引:0
|
作者
Wang, Chaowei [1 ,2 ]
Chen, Sijie [1 ,2 ]
Yuan, Yuequan [1 ,2 ]
Li, Shujin [1 ,2 ]
Lv, Xi [1 ,2 ]
Wu, Yifan [1 ,2 ,4 ]
Zhang, Yu [1 ,2 ,4 ]
Wang, Wei [3 ]
Ning, Yujie [1 ,2 ]
Wang, Xi [1 ,2 ,4 ]
机构
[1] Xi An Jiao Tong Univ, Hlth Sci Ctr, Sch Publ Hlth, Xian 710061, Shaanxi, Peoples R China
[2] Xi An Jiao Tong Univ, Collaborat Innovat Ctr Endem Dis & Hlth Promot Sil, NHC Key Lab Environm & Endem Dis, Xian 710061, Shaanxi, Peoples R China
[3] Inst Hyg Ordnance Ind, Ctr Occupat Safety & Hlth, Xian 710061, Shaanxi, Peoples R China
[4] Xi An Jiao Tong Univ, Hlth Sci Ctr, Sch Publ Hlth, Dept Occupat & Environm Hlth, Xian 710061, Shaanxi, Peoples R China
关键词
Kashin-Beck disease; Ferroptosis; Chondrocyte death; Selenium deficiency; T-2; toxin; GLUTATHIONE-PEROXIDASE; 4; EXPRESSION; MODEL; OSTEOARTHRITIS; CHONDROCYTES; APOPTOSIS; AUTOPHAGY; RATS;
D O I
10.1016/j.mehy.2024.111469
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Kashin-Beck disease (KBD) is a prevalent, endemic, and degenerative cartilage injury disorder, characterized by high rates of teratogenicity and disability. The etiology and pathogenesis of KBD are not fully understood, although research suggests that selenium deficiency and exposure to T-2 toxin are significant environmental risk factors. The initial pathological changes of KBD manifest as necrosis of deep chondrocytes, dedifferentiation of chondrocytes, excessive apoptosis of chondrocytes, and subsequent disruption of extracellular matrix metabolism. However, the precise pathogenic mechanisms of chondrocyte damage in KBD remain incompletely understood. Ferroptosis is a unique form of programmed cell death triggered by iron-dependent lipid peroxide accumulation. It has been shown to contribute to cartilage damage and chondrocyte death in various osteoarticular conditions, particularly osteoarthritis (OA). Notably, KBD not only exhibits clinical and pathological similarities with OA, but also indicates a potential association with ferroptosis in morphological and molecular similarities. Additionally, the environmental risk factors T-2 toxin exposure and selenium deficiency are also significant contributors to ferroptosis. Consequently, it is plausible to postulate that environmental risk factors may trigger ferroptosis, leading to the initiation of cartilage damage in KBD. Our hypothesis can be verified through both in vitro and in vivo experiments. Chondrocyte injury induced by ferroptosis may be a novel finding in KBD, which is important for clarifying its etiology and developing effective therapeutic strategies.
引用
收藏
页数:6
相关论文
共 50 条
  • [41] Whole-Transcriptome Sequencing of Knee Joint Cartilage from Kashin-Beck Disease and Osteoarthritis Patients
    Han, Lixin
    Cheng, Bolun
    Wei, Wenming
    Liu, Li
    Cheng, Shiqiang
    Liu, Huan
    Jia, Yumeng
    Wen, Yan
    Zhang, Feng
    INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2024, 25 (08)
  • [42] Promotion of the articular cartilage proteoglycan degradation by T-2 toxin and selenium protective effect
    Si-yuan Li
    Jun-ling Cao
    Zhong-li Shi
    Jing-hong Chen
    Zeng-tie Zhang
    Clare E. Hughes
    Bruce Caterson
    Journal of Zhejiang University SCIENCE B, 2008, 9 : 22 - 33
  • [43] Promotion of the articular cartilage proteoglycan degradation by T-2 toxin and selenium protective effect
    Li, Si-yuan
    Cao, Jun-ling
    Shi, Zhong-li
    Chen, Jing-hong
    Zhang, Zeng-tie
    Hughes, Clare E.
    Caterson, Bruce
    JOURNAL OF ZHEJIANG UNIVERSITY-SCIENCE B, 2008, 9 (01): : 22 - 33
  • [44] RETRACTION: LncRNA MIAT regulated by selenium and T-2 toxin increases NF-kappa B-p65 activation, promoting the progress of Kashin-Beck Disease (Retraction of Vol 40, Pg 869, 2020)
    Shi, M.
    He, Y.
    Zhang, Y.
    Guo, X.
    Lin, J.
    Wang, W.
    Chen, Jinghong
    HUMAN & EXPERIMENTAL TOXICOLOGY, 2022, 41
  • [45] The Role of Selenium-Mediated Notch/Hes1 Signaling Pathway in Kashin-Beck Disease Patients and Cartilage Injury Models
    Zhang, Di
    Zhang, Dandan
    Yang, Xiaoli
    Li, Qiang
    Zhang, Rongqiang
    Xiong, YongMin
    BIOLOGICAL TRACE ELEMENT RESEARCH, 2023, 201 (06) : 2765 - 2774
  • [47] SELENIUM DEFICIENCY AND FULVIC-ACID SUPPLEMENTATION INDUCES FIBROSIS OF CARTILAGE AND DISTURBS SUBCHONDRAL OSSIFICATION IN KNEE JOINTS OF MICE - AN ANIMAL-MODEL STUDY OF KASHIN-BECK DISEASE
    YANG, CL
    WOLF, E
    ROSER, K
    DELLING, G
    MULLER, PK
    VIRCHOWS ARCHIV A-PATHOLOGICAL ANATOMY AND HISTOPATHOLOGY, 1993, 423 (06) : 483 - 491
  • [48] Bcl-2 expression and apoptosis of chondrocyte in young rat and children with Kashin-Beck disease: Relationship with selenium
    Luo, ZG
    Dong, HY
    Gao, XQ
    Yu, SW
    Hu, P
    Huang, G
    Niu, YS
    BONE, 2005, 36 : S32 - S33
  • [49] RETRACTED: LncRNA MIAT regulated by selenium and T-2 toxin increases NF-κB-p65 activation, promoting the progress of Kashin-Beck Disease (Retracted article. See vol. 41, 2022)
    Shi, Min
    He, Ying
    Zhang, Ying
    Guo, Xiaobo
    Lin, Jing
    Wang, Wei
    Chen, Jinghong
    HUMAN & EXPERIMENTAL TOXICOLOGY, 2021, 40 (05) : 869 - 881
  • [50] Chondrocyte apoptosis and expression of Bcl-2, Bax, Fas, and NOS in articular cartilage in patients with Kashin-Beck disease
    Wang, SH
    Guo, X
    Zuo, H
    Zhang, YG
    Xu, P
    Ping, ZG
    Zhang, ZT
    Geng, D
    JOURNAL OF RHEUMATOLOGY, 2006, 33 (03) : 615 - 619