Liangyu Cui, Xi Wang, Chaowei Wang, Yang Liu, Lulu Bai, Lian Liu, Qi Jing, Yuyang Ma, Pengyan Jiao, Zhouyun Chen, Yirong Qin, Hui Wang, Yuequan Yuan, Xi Lyu, Yu Zhang, Xiong Guo, Yujie Ning, Feng Zhang
WHAT IS ALREADY KNOWN ABOUT THIS TOPIC?: Lipids are key mediators in cartilage degeneration. While T-2 toxin exposure drives Kashin-Beck disease (KBD), systematic metabolic comparisons between KBD and osteoarthritis (OA) are lacking.
WHAT IS ADDED BY THIS REPORT?: KBD and OA share cartilage lipid alterations linked to ferroptosis, but KBD exhibits unique changes indicating severe oxidative stress. Furthermore, prostaglandin-endoperoxide synthase 2 (PTGS2) was identified as the candidate molecular target potentially involved in T-2 toxin-induced cartilage damage.
WHAT ARE THE IMPLICATIONS FOR PUBLIC HEALTH PRACTICE?: Uncovering the adverse outcome pathway of T-2 toxin exposure clarifies KBD pathogenesis. Targeting the PTGS2-mediated signaling pathway may provide a potential strategy for clinical intervention and disease management.