Inhibiting ANP32E protects against acute kidney injury by regulating autophagy via the AMPK pathway
Summary: 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 a...
Saved in:
| Main Authors: | , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2025-08-01
|
| Series: | iScience |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2589004225012751 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| Summary: | Summary: 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. |
|---|---|
| ISSN: | 2589-0042 |