Inhibiting ANP32E protects against acute kidney injury by regulating autophagy via the AMPK pathway.

Ischemia-reperfusion (I/R) injury is a secondary injury that frequently occurs during acute kidney injury (AKI) treatment. Acidic nuclear phosphoprotein 32 family member E (ANP32E) disorders are associated with several pathological conditions linked to renal dysfunction. However, the role and mechanism of ANP32E in AKI remain unclear. An AKI mouse model was established by I/R. Additionally, we used microarray technology and in vitro assays to examine the molecular function of ANP32E. In this study, we found that ANP32E was increased in the I/R model. Knockdown of ANP32E promoted autophagy, further preventing kidney tubular cell apoptosis and improving renal function. Transcriptome sequencing indicated that suppressing ANP32E activated the AMP-activated protein kinase (AMPK)/autophagy signaling pathway. In summary, these findings suggest that ANP32E plays a role in pathogenesis and provide a new avenue for the treatment of acute ischemic kidney injury.