ArticleFrontiers in molecular biosciences2025
Exploring molecular characteristics and interactions of blood stasis syndrome in ischemic heart failure by integrated multi-omics.
Article in Frontiers in molecular biosciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Ischemic heart failure (IHF) is one of the leading causes of death worldwide. In traditional Chinese medicine, blood stasis syndrome (BSS) is regarded as a core pathological feature of IHF. This study aims to clarify the main biological characteristics and underlying mechanisms of BSS in IHF. Methods: Using an integrated multi-omics strategy combining transcriptomics, proteomics, and targeted metabolomics, we systematically analyzed the molecular characteristics of BSS in patients with IHF from multiple perspectives. By integrating multi-omics data and correlating them with clinical parameters, we identified a core molecular network associated with BSS. Key targets within this network were further validated using iPRM and RT-qPCR. ROC curve analysis and responses to pharmacological intervention were employed to confirm the diagnostic and therapeutic potential of these core molecular targets. Results: A total of 435 differentially expressed genes, 176 differentially abundant proteins, and 40 differentially altered metabolites related to IHF with BSS were identified. Multi-omics analysis highlighted the involvement of the complement and coagulation cascade and B cell receptor signaling pathway. Moreover, targeted metabolomics suggested that metabolic pathways associated with BSS involve glycine, arginine, tryptophan metabolism, and fatty acid biosynthesis. Integrated multi-omics correlation analysis identified CD79A, CD79B, CD19, CD22, CR2, F2, F8, F9, C3, FN1, 5-hydroxyindolacetic acid, and 4-acetamidobutanoate as core molecular features, with significant correlations observed between these molecules and clinical indicators. iPRM and RT-qPCR validation confirmed that the expression trends of these core molecules are consistent with the sequencing results. Furthermore, cross-validation with Yiqi Huoxue formula intervention identified F2, F8, F9, and FN1 as four diagnostic and therapeutic targets for BSS. Conclusion: This multi-omics analysis reveals that immune dysregulation, inflammation, and impaired coagulation function are central to BSS in IHF. Key pathways involved include the complement and coagulation cascade as well as B-cell receptor signaling, with F2, F8, F9, and FN1 identified as potential diagnostic and therapeutic targets. These findings provide new molecular insights into BSS in IHF.
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