Abstract:
Acute kidney injury (AKI)-to-chronic kidney disease (CKD) transition is a slow but persistent progression toward end-stage kidney disease. Earlier reports have shown that Hippo components, such as Yes-associated protein (YAP) and its homolog Transcriptional coactivator with PDZ-binding motif (TAZ), regulate inflammation and fibrogenesis during the AKI-to-CKD transition. Notably, the roles and mechanisms of Hippo components vary during AKI, AKI-to-CKD transition, and CKD. Hence, it is important to understand these roles in detail. This review addresses the potential of Hippo regulators or components as future therapeutic targets for halting the AKI-to-CKD transition.