Apelin-13 inhibits ischemia–reperfusion mediated podocyte apoptosis by reducing m-TOR phosphorylation to enhance autophagy

Podocytes are essential to maintain the normal filtration function of glomerular basement membrane, which could be injured by ischemia–reperfusion. As complicated function of autophagy in terminal differentiated podocytes, autophagy dysfunction might contribute to I/R induced renal dysfunction following glomerular filtration membrane (GFM) injuries. Meanwhile, apelin-13, an endogenous polypeptide, has been proved to be effective in regulating autophagy and apoptosis in podocytes. Therefore, it is hypothesized that apelin-13 may protect podocytes from IRI by inhibiting podocyte apoptosis through regulation of podocyte autophagy. Our study demonstrates for that podocytes are also involved in renal ischemia–reperfusion (I/R) injury and shows in detail the morphological and functional changes in podocytes during renal I/R. Because podocytes are terminally differentiated cells whose homeostasis require high levels of autophagy, we investigate the cellular mechanisms underlying the effects of apelin-13 on I/R-mediated podocyte injury in terms of autophagy. In addition, our study demonstrates that apelin-13 ameliorates renal I/R injury in podocyte injury, by increasing podocyte autophagy through inhibition of m-TOR phosphorylation, which in turn inhibits apoptosis.