ATG7 promotes autophagy in sepsis-induced acute kidney injury and is inhibited by miR-526b

Sepsis is considered to be the most common contributing factor in the development of acute kidney injury (AKI). However, the mechanisms by which sepsis leads to AKI remain unclear. Autophagy is important for a number of fundamental biological activities and plays a key role in numerous different diseases. The present study demonstrated that autophagy is involved in sepsis-induced kidney injury and upregulates ATG7, LC3 and Beclin I. In addition, it was revealed that miR-526b is decreased in sepsis-induced kidney injury, and miR-526b was identified as a direct regulator of ATG7. Furthermore, the present study investigated the biological effects of ATG7 inhibited by miR-526b and demonstrated that miR-526b could promote cell viability by inhibiting autophagy, potentially through targeting ATG7. In conclusion, the present study highlights the role of autophagy in sepsis-induced AKI, and miR-526b in regulating autophagy through targeting ATG7, which suggested that miR-526b may be a molecular therapeutic target for sepsis-induced AKI.