Zinc‑finger E‑box‑binding homeobox 1 alleviates acute kidney injury by activating autophagy and the AMPK/mTOR pathway.

Zinc‑finger E‑box‑binding homeobox 1 (ZEB1) is involved in epithelial‑mesenchymal transition. In the present study, the protective effect of ZEB1 on acute kidney injury (AKI) was explored. The cecal ligation and puncture (CLP) method was performed to establish the AKI model in rats. ZEB1 expression, blood urea nitrogen (BUN) and serum creatinine (SCr) levels, inflammation [interleukin (IL)‑1β, IL‑6, and tumour necrosis factor‑α], phosphorylated AMP‑activated protein kinase (p‑AMPK) and phosphorylated mammalian target of rapamycin (p‑mTOR) expression, and histopathological changes in CLP‑induced AKI rats were assessed. AMPK inhibitor dorsomorphin (DM) was intraperitoneally injected to determine the effect of ZEB1 on AKI and the regulatory mechanism involving the AMPK/mTOR pathway. CLP downregulated ZEB1 expression, increased BUN and SCr levels, promoted inflammation and apoptosis, and increased the acute kidney score in the kidney tissues of CLP‑induced AKI rats. Autophagy and the AMPK/mTOR pathway were blocked in CLP‑induced AKI rats. ZEB1 overexpression inhibited inflammation and apoptosis, reduced BUN and SCr levels, and activated autophagy and the AMPK/mTOR pathway in CLP‑induced AKI rats. The protective effect of ZEB1 overexpression on AKI was reversed by DM. Thus, ZEB1 was revealed to alleviate CLP‑induced AKI by activating autophagy and the AMPK/mTOR pathway.