Selenomethionine alleviates T-2 toxin-induced articular chondrocyte ferroptosis via the system Xc−/GSH/GPX4 axis

/GSH/GPX4 axis, thereby antagonizing ferroptosis of chondrocytes and alleviating articular cartilage damage. In conclusion, our findings highlight the essentiality of ferroptosis in chondrocyte caused by T-2 toxin, elucidate how Se-Met offers protection against this injury and provide research evidence for the drug treatment target of Kashin-Beck disease.