Autophagy upregulation ameliorates cell injury in Sequestosome 1 knockout podocytes in vitro.

Autophagy is a catabolic process to maintain intracellular homeostasis that degrades damaged proteins and organelles in mammalian cells. Podocytes are crucial for maintaining the normal function of the glomerular filtration barrier. In the present study, we aimed to investigate the high glucose-induced cell injury in human podocytes and the protective role of autophagy in this process. Here we show that the autophagy activity was decreased under the high glucose conditions and 72 h of high glucose exposure inhibited the cell viablity and aggravated cell injury. Moreover, autophagy upregulation by Sequestosome 1 (p62/SQSM1) knockdown ameliorated this cell injury and relieved insulin resistance. Collectively, the present study proposed a novel autophagy involved mechanism of high glucose-induced cell injury. The present study deepens our understanding of the role of autophagy in the pathogenesis of diabetic nephropathy and provided potential therapeutic strategy for diabetic nephropathy.