In this study, we collected serum from sepsis and healthy patients, constructed sepsis mouse models by cecal ligation and puncture (CLP) and stimulated mouse kidney epithelial TCMK-1 cells with LPS in vitro to investigate the role of miR-106a in sepsis-induced AKI and its related mechanisms, as well as the possible regulatory relationship with THBS2. Here, THBS2 is linked to Sepsis.