Matches in SemOpenAlex for { <https://semopenalex.org/work/W4366772610> ?p ?o ?g. }
- W4366772610 abstract "The chronic metabolic disease named type 2 diabetes (T2D) accounts for over 90% of diabetes mellitus. An increasing number of evidences have revealed that hypoxia has a significantly suppressive effect on cell-mediated immunity, as well as the utilization of glucose in diabetics. Therefore, we aimed to screen and identify hypoxia-immune-related hub genes in T2D through bioinformatic analysis. The Gene Expression Omnibus (GEO) database was used to get T2D gene expression profile data in the peripheral blood samples (GSE184050), and hypoxia-related genes were acquired from Molecular Signatures Database (MSigDB). Differentially expressed mRNAs (DEGs) and lncRNAs (DELs) between T2D and normal samples were identified by DeSeq2 package. The clusterProfiler package was used to perform enrichment analyses for the overlapped genes of DEGs and hypoxia-related genes. Further, Hypoxia-related hub genes were discovered using two machine learning algorithms. Next, the compositional patterns of immune and stromal cells in T2D and healthy groups were estimated by using xCell algorithm. Moreover, we used the weighted correlation network analysis (WGCNA) to examine the connection between genes and immune cells to screen immune-related genes. Gene Set Enrichment Analysis (GSEA) was used to investigate the functions of the hypoxia-immune-related hub genes. Finally, two peripheral blood cohorts of T2D (GSE184050 and GSE95849) as well as the quantitative real-time PCR (qRT-PCR) experiments for clicinal peripheral blood samples with T2D were used for verification analyses of hub genes. And meanwhile, a lncRNA-TF-mRNA network was constructed. Following the differentially expressed analysis, 38 out of 3822 DEGs were screened as hypoxia-related DEGs, and 493 DELs were found. These hypoxia-related DEGs were mainly enriched in the GO terms of pyruvate metabolic process, cytoplasmic vesicle lumen and monosaccharide binding, and the KEGG pathways of glycolysis/gluconeogenesis, pentose phosphate pathway and biosynthesis of nucleotide sugars. Moreover, 7 out of hypoxia-related DEGs were identified as hub genes. There were six differentially expressed immune cell types between T2D and healthy samples, which were further used as the clinical traits for WGCNA to identify AMPD3 and IER3 as the hypoxia-immune-related hub genes. The results of the KEGG pathways of genes in high-expression groups of AMPD3 and IER3 were mainly concentrated in glycosaminoglycan degradation and vasopressin-regulated water reabsorption, while the low-expression groups of AMPD3 and IER3 were mainly associated with RNA degradation and nucleotide excision repair. Finally, when compared to normal samples, both the AMPD3 and IER3 were highly expressed in the T2D groups in the GSE184050 and GSE95849 datasets. The result of lncRNA-TF-mRNA regulatory network showed that lncRNAs such as BACH1-IT1 and SNHG15 might induce the expression of the corresponding TFs such as TFAM and THAP12 and upregulate the expression of AMPD3. This study identified AMPD3 and IER3 as hypoxia-immune-related hub genes and potential regulatory mechanism for T2D, which provided a new perspective for elucidating the upstream molecular regulatory mechanism of diabetes mellitus." @default.
- W4366772610 created "2023-04-25" @default.
- W4366772610 creator A5012677271 @default.
- W4366772610 creator A5019018136 @default.
- W4366772610 creator A5041520008 @default.
- W4366772610 creator A5046124835 @default.
- W4366772610 creator A5069102353 @default.
- W4366772610 date "2023-04-21" @default.
- W4366772610 modified "2023-09-30" @default.
- W4366772610 title "Identification and analysis of hub genes of hypoxia-immunity in type 2 diabetes mellitus" @default.
- W4366772610 cites W1172574862 @default.
- W4366772610 cites W1559525331 @default.
- W4366772610 cites W1630376243 @default.
- W4366772610 cites W1753982827 @default.
- W4366772610 cites W1945308826 @default.
- W4366772610 cites W1966327575 @default.
- W4366772610 cites W1975388666 @default.
- W4366772610 cites W1976055428 @default.
- W4366772610 cites W1986197217 @default.
- W4366772610 cites W1991401793 @default.
- W4366772610 cites W2008792074 @default.
- W4366772610 cites W2018607502 @default.
- W4366772610 cites W2034097886 @default.
- W4366772610 cites W2037208645 @default.
- W4366772610 cites W2054537489 @default.
- W4366772610 cites W2072174276 @default.
- W4366772610 cites W2091725413 @default.
- W4366772610 cites W2120824707 @default.
- W4366772610 cites W2125435853 @default.
- W4366772610 cites W2145697808 @default.
- W4366772610 cites W2146512944 @default.
- W4366772610 cites W2149659037 @default.
- W4366772610 cites W2168528711 @default.
- W4366772610 cites W2179438025 @default.
- W4366772610 cites W2480256079 @default.
- W4366772610 cites W2522656345 @default.
- W4366772610 cites W2556833154 @default.
- W4366772610 cites W2558304416 @default.
- W4366772610 cites W2562967686 @default.
- W4366772610 cites W2625925390 @default.
- W4366772610 cites W2800009626 @default.
- W4366772610 cites W2901857397 @default.
- W4366772610 cites W2911351998 @default.
- W4366772610 cites W2945822310 @default.
- W4366772610 cites W2952001873 @default.
- W4366772610 cites W2996012059 @default.
- W4366772610 cites W2996626242 @default.
- W4366772610 cites W3107993577 @default.
- W4366772610 cites W3126701302 @default.
- W4366772610 cites W3130968559 @default.
- W4366772610 cites W3175752499 @default.
- W4366772610 cites W3194346210 @default.
- W4366772610 cites W4205657036 @default.
- W4366772610 cites W4206501402 @default.
- W4366772610 cites W4308786416 @default.
- W4366772610 cites W4315489863 @default.
- W4366772610 cites W4319462046 @default.
- W4366772610 cites W4321332887 @default.
- W4366772610 doi "https://doi.org/10.3389/fgene.2023.1154839" @default.
- W4366772610 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37153000" @default.
- W4366772610 hasPublicationYear "2023" @default.
- W4366772610 type Work @default.
- W4366772610 citedByCount "0" @default.
- W4366772610 crossrefType "journal-article" @default.
- W4366772610 hasAuthorship W4366772610A5012677271 @default.
- W4366772610 hasAuthorship W4366772610A5019018136 @default.
- W4366772610 hasAuthorship W4366772610A5041520008 @default.
- W4366772610 hasAuthorship W4366772610A5046124835 @default.
- W4366772610 hasAuthorship W4366772610A5069102353 @default.
- W4366772610 hasBestOaLocation W43667726101 @default.
- W4366772610 hasConcept C104317684 @default.
- W4366772610 hasConcept C150194340 @default.
- W4366772610 hasConcept C178790620 @default.
- W4366772610 hasConcept C185592680 @default.
- W4366772610 hasConcept C203014093 @default.
- W4366772610 hasConcept C2779341262 @default.
- W4366772610 hasConcept C540031477 @default.
- W4366772610 hasConcept C54355233 @default.
- W4366772610 hasConcept C60644358 @default.
- W4366772610 hasConcept C70721500 @default.
- W4366772610 hasConcept C7836513 @default.
- W4366772610 hasConcept C86803240 @default.
- W4366772610 hasConcept C8891405 @default.
- W4366772610 hasConceptScore W4366772610C104317684 @default.
- W4366772610 hasConceptScore W4366772610C150194340 @default.
- W4366772610 hasConceptScore W4366772610C178790620 @default.
- W4366772610 hasConceptScore W4366772610C185592680 @default.
- W4366772610 hasConceptScore W4366772610C203014093 @default.
- W4366772610 hasConceptScore W4366772610C2779341262 @default.
- W4366772610 hasConceptScore W4366772610C540031477 @default.
- W4366772610 hasConceptScore W4366772610C54355233 @default.
- W4366772610 hasConceptScore W4366772610C60644358 @default.
- W4366772610 hasConceptScore W4366772610C70721500 @default.
- W4366772610 hasConceptScore W4366772610C7836513 @default.
- W4366772610 hasConceptScore W4366772610C86803240 @default.
- W4366772610 hasConceptScore W4366772610C8891405 @default.
- W4366772610 hasFunder F4320321001 @default.
- W4366772610 hasLocation W43667726101 @default.
- W4366772610 hasLocation W43667726102 @default.
- W4366772610 hasLocation W43667726103 @default.