American heart journal plus : cardiology research and practice · 2026
Mechanisms of gut microbiota metabolite-mediated gut-heart Axis in heart failure: An integrative study based on network pharmacology.
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Tan Feng, Cheng Yuan, Yan Jianwei, Zheng Zeqi
Аннотация
BACKGROUND: Heart failure (HF) is a prevalent terminal-stage cardiovascular disease worldwide. Recent years have seen growing research on the gut-heart axis, yet the role of gut microbiota-derived metabolites in HF pathogenesis remains insufficiently explored.
METHODS: This network pharmacology study screened overlapping targets of heart failure and gut metabolites via gutMGene, GeneCards and OMIM databases, then carried out PPI, enrichment, M-S-M-T network construction, as well as drug-likeness and toxicity prediction of metabolites.
RESULTS: We identified 47 candidate targets at the intersection of HF-related genes and gut metabolite-associated targets. PPI network analysis suggested that AKT1, TNF, TP53, IL6, and PPARG may represent key hub targets. Functional enrichment indicated potential associations with the NF-κB and PI3K-Akt signaling pathways. The M-S-M-T regulatory network results show that PPARG is the hub target with the most extensive connections. Drug-likeness and toxicity predictions suggested favorable in silico profiles for five metabolites, including 3-indolepropionic acid (IPA) and indole-3-lactic acid (ILA).
CONCLUSION: This network pharmacology study screened core genes, metabolites and pathways associated with the gut-heart axis in heart failure, providing hypothetical support for subsequent experimental research on intervening heart failure via gut microbiota-derived metabolites.
METHODS: This network pharmacology study screened overlapping targets of heart failure and gut metabolites via gutMGene, GeneCards and OMIM databases, then carried out PPI, enrichment, M-S-M-T network construction, as well as drug-likeness and toxicity prediction of metabolites.
RESULTS: We identified 47 candidate targets at the intersection of HF-related genes and gut metabolite-associated targets. PPI network analysis suggested that AKT1, TNF, TP53, IL6, and PPARG may represent key hub targets. Functional enrichment indicated potential associations with the NF-κB and PI3K-Akt signaling pathways. The M-S-M-T regulatory network results show that PPARG is the hub target with the most extensive connections. Drug-likeness and toxicity predictions suggested favorable in silico profiles for five metabolites, including 3-indolepropionic acid (IPA) and indole-3-lactic acid (ILA).
CONCLUSION: This network pharmacology study screened core genes, metabolites and pathways associated with the gut-heart axis in heart failure, providing hypothetical support for subsequent experimental research on intervening heart failure via gut microbiota-derived metabolites.