Progress on the mechanism of cartilage damage induced by T-2 toxin in Kashin-Beck disease

VernacularTitle:T-2毒素致大骨节病软骨损伤机制的研究进展
Author: Cong YAO ¹ ; Shuichu HAO ; Chun ZHANG ; Jun DONG ; Yumeng JIA ; Xiong GUO
Author Information

1. 西安交通大学第二附属医院　陕西省地方病临床医学研究中心，西安　710004
Keywords: T-2 toxin; Immunotoxicity; Apoptosis; Oxidative stress; Kashin-Beck disease
From: Chinese Journal of Endemiology 2024;43(5):421-424
CountryChina
Language:Chinese
Abstract: Kashin-Beck disease (KBD) is an endemic and degenerative osteoarthropathy that can cause damage to the endochondral ossification of the limbs during development. The etiology is still unclear. In recent years, scholars at home and abroad have studied the mechanism of T-2 toxin and its metabolites causing KBD cartilage damage from the perspectives of immunotoxicity, oxidative stress, inflammatory response, cell apoptosis, etc., mainly including transforming growth factor-β receptor (TGF-βRs) signaling pathway, immune regulatory factor, inflammatory factor IL-1β and apoptosis enzyme activating factor 1 (APAF1), which promote the progression of KBD by inducing human chondrocyte injury, inhibiting matrix synthesis and accelerating cellular catabolism. This article reviews the research progress on the immunotoxicity of T-2 toxin and its toxic effects on KBD cartilage injury at the molecular level, in order to provide a scientific basis for prevention and treatment of KBD.