miR-214 ameliorates sepsis-induced acute kidney injury via PTEN/AKT/mTOR-regulated autophagy

Previous studies have suggested that oxidative stress and autophagy results in acute kidney injury (AKI) during sepsis and microRNA (miR)-214 serves a vital role in the protection of kidneys subjected to oxidative stress. The present study aimed to test whether the renoprotection of miR-214 is related to autophagy in sepsis. The role of autophagy was investigated in a mouse model of cecal ligation and puncture (CLP). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to analyze the expression of miR-214. The structure and function of kidneys harvested from the mice were evaluated. Kidney autophagy levels were detected with immunohistochemical, immunofluorescent and western blotting. It was found that miR-214 could alleviate AKI in septic mice by inhibiting the level of kidney autophagy. Furthermore, miR-214 inhibited autophagy by silencing PTEN expression in the kidney tissues of septic mice. These findings indicated that miR-214 ameliorated CLP-induced AKI by reducing oxidative stress and inhibiting autophagy through the regulation of the PTEN/AKT/mTOR pathway.

Automated summary

The study demonstrated that miR-214 alleviated AKI in septic mice by inhibiting kidney autophagy levels. miR-214 further inhibited autophagy by silencing PTEN expression in the kidney tissues of septic mice. These results suggest that miR-214 ameliorated CLP-induced AKI by reducing oxidative stress and inhibiting autophagy through the regulation of the PTEN/AKT/mTOR pathway.