Fig 2: Metabolic profile changes in heart valve with calcific aortic valve disease. Principal component analysis (A) and PLS-DA (B) score plots; permutation test of PLS-DA model (C). OPLS-DA score of positive and negative ion metabolites plots (D). OPLS-DA, orthogonal projections to latent structures discriminant analysis; PCA, principal component analysis; PLS-DA, partial least squares discriminant analysis.

Fig 3: The GSEA enrichment analysis of ENPP1 differentially expressed genes in LIHC. (a-f) The fatty acid metabolism, nonalcoholic fatty liver disease, fatty acids omega oxidation, fatty acyl COA biosynthesis, fatty acid biosynthesis, and the biosynthesis of unsaturated fatty acid pathways were enriched in ENPP1 differentially expressed genes in LIHC.

Fig 4: Levels of hub metabolites and proteins. Boxplots show levels of panels (A–G) hub metabolites ADP, D-glucose 1-phosphate, L-aspartic acid, L-dopa, oxoglutaric acid, rotenone, and sorbitol and (H–L) hub proteins ENPP1, CAMK2D, ABCA8, SLC2A1, and NDUFA12 in CAVD and control samples. *P < 0.05; **P < 0.01; ***P < 0.001 vs. control. ABCA8, ATP Binding Cassette Subfamily A Member 8, CAMK2D, calcium2 + /calmodulin-dependent protein kinase II delta; ENPP1, ectonucleotide pyrophosphatase/phosphodiesterase 1NDUFA12, NADH:ubiquinone oxidoreductase subunit A12; SLC2A, solute carrier family 2 member 1.

Fig 5: The effect of IL1RAP and ENPP1 on the patients' prognosis in LIHC. (a-b) The Kaplan–Meier plotter database indicated the prognostic values of aberrantly expressed IL1RAP and ENPP1 in LIHC patients, including overall survival and disease-specific survival.