These results indicate that AT1 expression is enhanced, at least in part, by 12-LO in the type 2 diabetic glomeruli, and 12-LO inhibition can ameliorate DN progression through downregulation of AT1 expression.

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Diabetes is a leading cause of death and disability. In 2004, 3.4 million people worldwide died of symptoms relating to high blood sugar. Diabetic complications are caused by organ damage resulting from long-term exposure to high blood sugar, and include diseases such as heart failure, kidney failure, vision loss and neuropathy. The transcription factor nuclear factor (erythroid-derived 2)-like 2 (NFE2L2, also known as NRF2) is an important component of the intracellular antioxidant machinery and a target for treatment of diabetic complications. This article reviews the role of NFE2L2 in diabetic complications with a focus on diabetic nephropathy, cardiomyopathy, neuropathy and retinopathy. Activation of NFE2L2 protects against oxidative stress in vitro and in vivo, and represents an important target for prophylaxis and treatment of diabetic complications. NFE2L2 has potential clinical applications for diabetic patients in the near future.

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In order to further elucidate the potential correlations and treatments of IgA nephropathy (IgAN) and hypertensive nephropathy (HT), bioinformatics analysis of IgAN and HT was performed. The mRNA expression profiles of human renal biopsy samples from patients with IgAN, patients with HT and pre-transplant healthy living controls (LD) were downloaded from the Gene Expression Omnibus database. Then, the differentially expressed genes (DEGs) were identified and functions of DEGs were analyzed. Finally, the regulatory networks containing DEGs and related-transcription factors (TFs) were constructed using Cytoscape software. When compared with the LD group, 134 and 188 DEGs were obtained in the IgAN and HT groups, respectively. A total of 39 genes were altered in the HT group when compared with the IgAN group. In addition, 66 genes were shared in the IgAN and HT groups when compared with the LD group, 6 of which [early growth response 1, activating transcription factor 3, nuclear receptor subfamily 4 group A member 2 (NR4A2), NR4A1, v-maf avian musculoaponeurotic fibrosarcoma oncogene homolog F and Kruppel like factor 6] were identified as TFs. In addition, DEGs including interleukin (IL) 1 receptor antagonist, collagen type 4 α2 chain, IL8, FBJ murine osteosarcoma viral oncogene homolog and somatostatin were enriched in a number of inflammation-associated biological processes, and DEGs including structural maintenance of chromosomes protein 3, v-crk avian sarcoma virus CT10 oncogene homolog and myosin 6 were enriched in non-inflammation-associated biological processes. Therefore, the differentially expressed TF genes and the genes associated with inflammation may be effective as potential therapeutic targets for IgAN and HT.