Objective: Atherosclerosis (AS) is the main pathological basis of most cardiovascular diseases, numerous studies have shown that programmed cell death and lncRNA-miRNA-mRNA regulatory network play an important role in cardiovascular diseases. However, the crosstalk between the ceRNA network associated with programmed cell death and AS remains unclear. This article aims to explore the role of programmed cell death-related ceRNA network in the pathophysiological process of AS, in order to provide new targets for the diagnosis and treatment of AS.: Methods: Firstly, the GSE97210 and GSE28858 datasets were screened from the GEO database, and the differentially expressed lncRNA, mRNA and miRNA were screened, and then the lncRNA-miRNA-mRNA regulatory network was constructed in Cytoscape 3.7.2 software based on ceRNA theory. Second, GO and KEGG enrichment analysis of mRNA in the ceRNA network was performed. Finally, the mRNAs in the ceRNA network were intersected with genes related to autophagy, pyroptosis and ferroptosis to construct a ceRNA network related to programmed cell death: Results: According to the results of bioinformatics analysis, a total of 1208 DElncRNAs, 4723 DEmRNAs and 139 DEmiRNAs were obtained. A ceRNA network consisting of 64 lncRNAs, 8 miRNAs and 167 mRNAs was constructed. The mRNAs in the CeRNA network are mainly enriched in biological functions such as positive regulation of transcription and migration, protein binding, GTPase activity, and signaling pathways such as PI3K-Akt signaling pathway, ErbB signaling pathway, and mTOR signaling pathway. Validated by receiver operating characteristic (ROC) curves, 7 lncRNA-mediated ceRNA regulatory pathways for pyroptosis and 23 lncRNA-mediated regulatory pathways for ferroptosis and autophagy were constructed.: Conclusion: This study screened and identified the lncRNA, miRNA and mRNA expression profiles specifically expressed in AS tissues based on bioinformatics analysis, and constructed a ceRNA network related to programmed cell death, which is helpful for us to understand that programmed cell death leads to AS The mechanism of action, while providing new insights into programmed cell death in AS.:
Background To explore the relationship between obesity and hypertension using bioinformatics analyses. Methods Disease databases (GeneCards, OMIM, CTD, TTD, DisGeNET, and Drugbank) were used to obtain hypertension and obesity-related targets. The intersection targets of obesity and hypertension were constructed using Venn diagrams. STRING online platform was used to obtain protein–protein interaction networks of common targets, and Cytohubba plug-in was used to screen the core targets. Gene ontology (GO) analysis and the enrichment analysis of Kyoto encyclopedia of genes and genomes (KEGG) were carried out using DAVID database. Results A total of 459 and 551 targets were obtained for obesity and hypertension, respectively. Among them, 135 were targets for both obesity and hypertension in which tumor necrosis factor (TNF), cell tumor antigen p53 (TP53), chemokine 2 (CCL2), Toll-like receptor 4 (TLR4), interleukin (IL) 1B, nitric oxide synthase 3 (NOS3), IL-6, and serine/threonine protein kinase 1 (AKT1) were key targets for regulating obesity and hypertension. Enrichment analysis yielded 306 GO entries [P < 0.05, false discovery rate (FDR) <0.05], which were involved in positive regulation of mitogen-activated protein kinase (MAPK) cascade, positive regulation of nitric oxide biosynthetic process, cilium basal body, hormone activity, and RNA polymerase II repeating transcription factor binding. The 86 enriched KEGG entries (P < 0.05, FDR <0.05) included adipocytokine signaling pathway, regulation of lipolysis in adipocytes, PI3K–Akt signaling pathway and forkhead transcription factor O (FoxO) signaling pathway. Conclusions TNF, TP53, CCL2, TLR4, IL-1B, NOS3, IL-6, AKT1, and the key pathways including adipocytokine signaling pathway, regulation of adipocyte lipolysis, PI3K–Akt and FoxO signaling pathway play a regulatory role in interactions between obesity and hypertension. These findings provide new insights into the complex interactions between obesity and hypertension.
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.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.