Lipidomic and transcriptomic reveals glycerophospholipid and sphingolipid disorders in CVB3 induced viral myocarditis.

Lipids, which possess a variety of physiological functions, have been demonstrated to be involved in the development of CVB3-induced viral myocarditis (VM). Nevertheless, the dynamic changes of lipid in VM, along with the underlying mechanisms, still require clarification. In our study, the serum and heart lipidomics in both the NC and VM groups was performed by LC-MS/MS. Univariate and multivariate statistical analyses were employed to identify the differential lipids between groups. The heart samples were further tested by the transcriptomic analysis to find the expression profile changes of genes involved in lipid metabolism. Totally, 628 differential lipids in the heart and 666 in the serum were selected based on the criteria of VIP > 1.0, P < 0.05, and fold change >1 or < 1, respectively. Glycerophospholipids (GP) and sphingolipids (SP) were identified as the primary differential lipids, suggesting a marked imbalance in the corresponding lipid metabolic pathways that may be involved in the progression of VM. Simultaneously, the transcriptional profile proved that differentially expressed genes (DEGs) were significantly enriched in GP and SP metabolism pathways. In the serum, the GP category members DLCL (20:5/22:6) and CL (23:1/18:0/22:4/22:6), as well as the SP category members Hex2Cer (d18:2/24:0) and SPHP (d20:1), exhibited a two-fold change. Collectively, combined with transcriptomics and lipidomics data suggest that CVB3 exert its destructive effect on heart possibly by regulating GP and SP metabolism pathways. Several lipids in serum may serve as potential indicators for the progression of VM.