Activation of autophagy contributes to the renoprotective effect of postconditioning on acute kidney injury and renal fibrosis.

Ischemia/Reperfusion injury contributes to acute kidney injury (AKI) and subsequent chronic kidney disease (CKD) including renal fibrosis. Autophagy is a cytoplasmic components degradation pathway that has complex function in the development of various diseases such as fibrosis in kidney. Our previous work demonstrated that postconditioning (POC) showed excellent therapeutic effect on renal fibrosis via inhibiting the overproduction of reactive oxygen species (ROS) after reperfusion. But the connection of autophagy and POC in the renoprotective effect remains unclear. Here, we defined the relevance of autophagy and POC in the protective effect on AKI and subsequent renal fibrosis. We found that at two days after I/R injury, POC largely reduced renal tubular epithelial cell apoptosis and improved renal function; autophagy was significantly activated in kidneys of the POC rats. At two months after reperfusion, the I/R injury rats displayed severe renal fibrosis and epithelial-mesenchymal transition (EMT), whereas these were remarkably attenuated in the POC treated rats. Overall, our results demonstrated that POC could reduce renal damage and attenuate the degree of EMT after I/R injury via enhanced activation of autophagy.