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• W4382631750 startingPage "372" @default.
• W4382631750 abstract "BACKGROUND: Vascular smooth muscle cells are key players involved in atherosclerosis, the underlying cause of coronary artery disease. They can play either beneficial or detrimental roles in lesion pathogenesis, depending on the nature of their phenotypic changes. An in-depth characterization of their gene regulatory networks can help better understand how their dysfunction may impact disease progression. METHODS: We conducted a gene expression network preservation analysis in aortic smooth muscle cells isolated from 151 multiethnic heart transplant donors cultured under quiescent or proliferative conditions. RESULTS: We identified 86 groups of coexpressed genes (modules) across the 2 conditions and focused on the 18 modules that are least preserved between the phenotypic conditions. Three of these modules were significantly enriched for genes belonging to proliferation, migration, cell adhesion, and cell differentiation pathways, characteristic of phenotypically modulated proliferative vascular smooth muscle cells. The majority of the modules, however, were enriched for metabolic pathways consisting of both nitrogen-related and glycolysis-related processes. Therefore, we explored correlations between nitrogen metabolism-related genes and coronary artery disease–associated genes and found significant correlations, suggesting the involvement of the nitrogen metabolism pathway in coronary artery disease pathogenesis. We also created gene regulatory networks enriched for genes in glycolysis and predicted key regulatory genes driving glycolysis dysregulation. CONCLUSIONS: Our work suggests that dysregulation of vascular smooth muscle cell metabolism participates in phenotypic transitioning, which may contribute to disease progression, and suggests that AMT (aminomethyltransferase) and MPI (mannose phosphate isomerase) may play an important role in regulating nitrogen and glycolysis-related metabolism in smooth muscle cells." @default.
• W4382631750 created "2023-07-01" @default.
• W4382631750 creator A5012383016 @default.
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• W4382631750 date "2023-08-01" @default.
• W4382631750 modified "2023-10-05" @default.
• W4382631750 title "Network Preservation Analysis Reveals Dysregulated Metabolic Pathways in Human Vascular Smooth Muscle Cell Phenotypic Switching" @default.
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• W4382631750 cites W1966327575 @default.
• W4382631750 cites W1966971152 @default.
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• W4382631750 cites W1993789860 @default.
• W4382631750 cites W1995213405 @default.
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• W4382631750 cites W2036897871 @default.
• W4382631750 cites W2044124287 @default.
• W4382631750 cites W2060705109 @default.
• W4382631750 cites W2071383658 @default.
• W4382631750 cites W2072245877 @default.
• W4382631750 cites W2080201763 @default.
• W4382631750 cites W2080460005 @default.
• W4382631750 cites W2094630733 @default.
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• W4382631750 doi "https://doi.org/10.1161/circgen.122.003781" @default.
• W4382631750 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37387208" @default.
• W4382631750 hasPublicationYear "2023" @default.
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