Key result
Eight downregulated glycolytic genes show potential as biomarkers for dilated cardiomyopathy.
Why the study?
Despite the crucial role of energy metabolism in cardiac function, therapeutic targets for key genes in dilated cardiomyopathy energy metabolism remain scarce.
Bioinformatics analysis reveals eight glycolysis-related genes that are downregulated in dilated cardiomyopathy and may serve as novel diagnostic and therapeutic targets.
May support diagnostic biomarkers in dilated cardiomyopathy; leaves open clinical validation and therapeutic targeting.
Background: Dilated cardiomyopathy (DCM) is a prevalent condition with diverse etiologies, including viral infection, autoimmune response, and genetic factors. Despite the crucial role of energy metabolism in cardiac function, therapeutic targets for key genes in DCM’s energy metabolism remain scarce. Methods: Our study employed the GSE79962 and GSE42955 datasets from the Gene Expression Omnibus (GEO) database for myocardial tissue sample collection and target gene identification via differential gene expression screening. Using various R packages, GSEA software, and the STRING database, we conducted data analysis, gene set enrichment, and protein-protein interaction predictions. The least absolute shrinkage and selection operator (LASSO) and Support Vector Machine (SVM) algorithms aided in feature gene selection, while the predictive model’s efficiency was evaluated via the receiver operating characteristic (ROC) curve analysis. We used the non-negative matrix factorization (NMF) method for molecular typing and the cell-type identification by estimating relative subsets of RNA transcripts (CIBERSORT) algorithm for predicting immune cell infiltration. Results: The DLAT and LDHA genes may regulate the immune microenvironment of DCM by influencing activated dendritic cells, activated mast cells, and M0 macrophages, respectively. The BPGM, DLAT, PGM2, ADH1A, ADH1C, LDHA, and PFKM genes may regulate m6A methylation in DCM by affecting the ZC3H13, ALKBH5, RBMX, HNRNPC, METTL3, and YTHDC1 genes. Further regulatory mechanism analysis suggested that PFKM, DLAT, PKLR, PGM2, LDHA, BPGM, ADH1A, and ADH1C could be involved in the development of cardiomyopathy by regulating the Toll-like receptor signaling pathway. Conclusions: PFKM, DLAT, PKLR, PGM2, LDHA, BPGM, ADH1A, and ADH1C may serve as potential targets for guiding the diagnosis, treatment, and follow-up of DCM.
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Chen et al. (2023) studied Dilated cardiomyopathy (n=37). Glycolysis-related genes (PFKM, DLAT, PKLR, PGM2, LDHA, BPGM, ADH1A, ADH1C) vs. Normal myocardial tissue was evaluated on Differential gene expression and diagnostic efficacy (AUC). Eight glycolytic genes were downregulated in dilated cardiomyopathy tissues and demonstrated potential as diagnostic biomarkers with AUC values ranging from 0.700 to 0.839.
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