The current work attempts to investigate the possible role of Cofilin-1 in AKI and potential molecular mechanism using an oxygen-glucose-deprivation (OGD)-induced AKI and mouse AKI models in vivo, and elucidate how Cofilin-1 upregulation could render AKI and related cellular defects, supporting the notion that Cofilin-1 is a candidate marker and therapeutic target of AKI. This evidence concerns the gene CFL1 and acute kidney injury.