GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE307nnn/GSE307956/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE307956GEOGSEfalseDJ-1 alleviates high glucose-induced podocyte injury via activating ERK1/2 signalingDiabetic nephropathy (DN) is one of the most common complications of diabetes. 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. Furthermore, the accumulation of p-ERK1/2 in the nucleus activated the ERK1/2 pathway and enhanced the expression of NF-κB p65 and AP-1, which inhibited the apoptosis of HPC in the high glucose milieu. In conclusion, our study demonstrated that high glucose decreased DJ-1 expression in HPC and that overexpression of DJ-1 attenuated the apoptosis of HPC in high glucose conditions via enhancing the ERK1/2 pathway and the expression of NF-κB p65 and AP-1. Our study provides a novel mechanism by which DJ-1 alleviates high glucose-induced podocyte injury.2026/04/22GSE307956GSM9234609GSM9234606GSM9234605GSM9234608GSM9234607GSM9234602GSM9234601GSM9234604GSM923460334284307956Homo sapiens[41996356]