Front Physiol. 2026 Aug 17;17:1837224. doi: 10.3389/fphys.2026.1837224. eCollection 2026.
ABSTRACT
BACKGROUND: Gut microbiota plays a significant role in the occurrence and progression of multisystem disease. Previous studies have indicated that the intestinal microenvironment is closely linked to metabolic and cardiovascular diseases, yet its underlying mechanism remains unclear. We aimed to explore the association between the gut microbiota-metabolite network and cardiovascular function with the transcriptomic changes in the myocardium of acute myocardial infarction (AMI) mice.
METHODS: Eight-week-old C57BL/6J mice were adaptively fed for 7 days and then divided into the AMI model group and Sham group. After surgery, multiple approaches were used to assess the physiological and pathological changes in mice. At 7 days post-surgery, cardiac sections were analyzed using H&E staining and Masson staining. The gastrointestinal contents collected from the AMI and Sham group mice were analyzed by 16S rRNA sequencing and untargeted metabolomics and apical myocardial tissues were harvested for transcriptomic detection. followed by multi-omics association analysis between the differential gut microbiota and metabolites. Taking metabolites as the bridge, an integrated multi-omics correlation analysis was conducted.
RESULTS: Compared with the Sham group, mice in the AMI group exhibited obvious myocardial pathological damage and significant depletion of gut microbiota such as Christensenellaceae_R-7_group, Allobaculum, and Akkermansia. These changes may be associated with regulation of pathways such as retrograde endocannabinoid signaling, glycerophospholipid metabolism, riboflavin metabolism and primary bile acid biosynthesis, and metabolites such as nitrogen/aromatic metabolites, phospholipid metabolites, and oxidative stress related metabolites. Myocardial transcriptomic results revealed that genes such as Sdha, Hadha and Hsdl2 were significantly downregulated in the AMI group, and the DEGs were highly enriched in pathways including fatty acid β-oxidation, mitochondrial respiratory chain and ATP metabolism, suggesting severe energy metabolism disorder in the myocardium of AMI mice.
CONCLUSIONS: Myocardial injury in AMI may show a link between the remodeling of gut microbial structure. Correlative correlations indicate that altered gastrointestinal metabolites, as products of gut microbiota, are closely associated with myocardial metabolic reprogramming after AMI, whereas causal effects remain to be verified by further functional experiments.
PMID:42676332 | PMC:PMC13526554 | DOI:10.3389/fphys.2026.1837224