ABSTRACT
Kashin-Beck disease (KBD) is an endemic, disabling and deforming osteoarthropathy and mainly affects children or teenagers in growth and development period. Screening of KBD susceptibility genes and related functional experiments were conducted to examine the relationship between the molecular mechanism of selenium (Se) and selenoprotein on chondrocyte oxidative stress, inflammation and apoptosis-signaling pathways. The oxidative damage effects on apoptosis and oxidative stress and inflammation signaling pathways in chondrocyte were observed in the model to explore for the protective mechanism of Se. GPX3 and DIO3 hypermethylation were associated with an increased risk of KBD. The selenoproteins mainly exhibited biological roles related to redox reactions, such as response to oxidative stress, response to reactive oxygen species, response to lipid hydroperoxide. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathways of selenoprotein family were analyzed by enrichment analysis.
