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.