Background: In recent years, it has been demonstrated that ferroptosis can be involved in a variety of kidney injury processes, but the role played by ferroptosis in hypertensive kidney injury is still unclear. The aim was to explore the mechanism of ferroptosis playing a role in hypertensive kidney disease and related signalling pathways.Methods: GSE37455 microarray data was downloaded from the Gene Expression Omnibus (GEO) database and preprocessed. Batch correction and differential analysis were performed on the normal population and the hypertensive nephropathy samples using the "sva" and "limma" packages in R software.Ferroptosis-related genes were obtained from the FerrDb database and normalized and processed using UniProt. Ferroptosis-related differentially expressed genes were obtained using Venny 2.1. and imported into the Search Tool for the Retrieval of Interacting Genes (STRING) to obtain protein-protein interactions (PPIs). The data were imported into Cytoscape 3.7.2 for processing to identify the core differential genes of ferroptosis based on nodes. Gene set enrichment analysis (GSEA) was performed on the core differential genes of ferroptosis to infer the pathway of ferroptosis action in hypertensive nephropathy.
Results:The R software processing yielded 37 differential genes, including 13 upregulated genes and 24 downregulated genes. 202 ferroptosis-related genes were obtained by screening, and 3 ferroptosis-related differentially expressed genes were obtained after taking the intersection. The ferroptosis-related core differentially expressed gene albumin (ALB) was obtained by PPI network analysis and Cytoscape processing.GSEA analysis revealed that ferroptosis may act in hypertensive nephropathy through pathways such as drug metabolism-cytochrome P450, branched-chain amino acid (BCAA) metabolism, retinol metabolism, and biological processes (BPs) such as organic and amino acid metabolism and humoral immunity.Conclusions: Ferroptosis may act in the development of hypertensive nephropathy through pathways such as BCAA metabolism and retinol metabolism and BPs such as organic and amino acid metabolism and humoral immunity.
Recently, GaTe and C2N monolayers have been successfully synthesized and show fascinating electronic and optical properties. Such hybrid of GaTe with C2N may induce new novel physical properties. In this work, we perform ab initio simulations on the structural, electronic, and optical properties of the GaTe/C2N van der Waals (vdW) heterostructure. Our calculations show that the GaTe/C2N vdW heterostructure is an indirect-gap semiconductor with type-II band alignment, facilitating an effective separation of photogenerated carriers. Intriguingly, it also presents enhanced visible-UV light absorption compared to its components and can be tailored to be a good photocatalyst for water splitting at certain pH by applying vertical strains. Further, we explore specifically the adsorption and decomposition of water molecules on the surface of C2N layer in the heterostructure and the subsequent formation of hydrogen, which reveals the mechanism of photocatalytic hydrogen production on the 2D GaTe/C2N heterostructure. Moreover, it is found that in-plane biaxial strains can induce indirect-direct-indirect, semiconductor-metal, and type II to type I or type III transitions. These interesting results make the GaTe/C2N vdW heterostructure a promising candidate for applications in next generation of multifunctional optoelectronic devices.Electronic supplementary materialThe online version of this article (10.1186/s11671-018-2708-x) contains supplementary material, which is available to authorized users.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.