Both in vitro and in vivo experiments demonstrated that hub ARDS-ARDEGs (SMARCD3 and TCN1,but not RPL14) significantly affected mitochondrial function, oxidative stress, apoptosis, glucose metabolism and inflammatory cytokine expression, offering new insights into potential mechanisms underlying ARDS and providing valuable information for optimizing clinical treatment strategies. This evidence concerns the gene SMARCD3 and acute respiratory distress syndrome.