Abstract
Acute kidney injury (AKI) is a progressive renal injury with high morbidity and mortality, however, the mechanism is far from being clarified and effective clinical interventions are lacking. USP36 is a deubiquitination enzyme involved in a variety of cellular biological processes, but its involvement in renal cell apoptosis and kidney disease is largely unknown. In the present study, we confirmed the decreased expression of USP36 both in vivo in mouse and human AKI samples and in vitro ischemic human renal proximal tubular cells, which are extremely sensitive to the damage of ischemic injury. Importantly, we found that overexpression of USP36 markedly decreased ischemia-induced apoptosis and oxidative stress in HK-2 cells, which was accompanied by elevated c-Myc and SOD2 protein levels with alleviated ischemia-induced ubiquitination of both proteins. Our findings revealed a novel role of USP36 in inhibiting apoptosis of human renal tubular cells induced by ischemia, and provided a potential therapeutic target for AKI treatment.