Autophagosome protects proximal tubular cells from aldosterone-induced senescence through improving oxidative stress

Aldosterone exerts an enormous function on proximal tubular cells (PTC) senescence, which is a common pathomechanism contributing to renal dysfunction. Numerous studies have shown that oxidative stress deeply involved in the pathophysiologic processes of chronic kidney diseases. The study aims investigate whether autophagy could regulate process senescence through PTC both vivo and ex vivo. Our results suggested aldosterone treatment increased as evidenced by percent SA-β-Gal positive cells, reactive oxygen species level, expression NADPH oxidase 4 (NOX4) rather than NOX2, up-regulation p21 cultured PTC. Furthermore, alternation p62 LC3-II/LC3-I demonstrated remarkably influenced autophagic flux. NOX4 siRNA or induction with rapamycin reduced aldosterone-induced On contrary, inhibition chloroquine worsened these changes. Similar were further confirmed may become realistic therapeutic strategy against injury via improving stress.