DJ-1 alleviates high glucose-induced podocyte injury via activating ERK1/2 signaling

DJ-1 has been reported to participate in the response to renal ischemia/reperfusion (I/R) injury. However, the underlying mechanisms of DJ-1 in the regulation of high glucose-induced renal injury remain obscure.

In this study, we performed RNA-seq to explore the function of high glucose on human podocyte cells (HPC), and found that high glucose widely regulated a variety of signaling pathways, including cell growth and death, signal transduction, etc. Furthermore, we found that DJ-1 was decreased in the high glucose conditions and DJ-1 could attenuate the high glucose-induced HPC apoptosis. Mechanically, overexpression of DJ-1 increased the phosphorylation of ERK1/2 (p-ERK1/2) and then mediated the transport of p-ERK1/2 from the cytoplasm to the nucleus.