Key result
Genetically predicted Faecalibacterium abundance is linked to less myocardial interstitial fibrosis, mediated by plasma sphingomyelin.
Why the study?
Although associations between gut microbiota and myocardial interstitial fibrosis were established, causal relationships and potential intermediaries remained unknown.
Does genetic predisposition to specific gut microbiota causally influence myocardial interstitial fibrosis?
Observational (n=41,505)
Does genetic predisposition to specific gut microbiota causally influence myocardial interstitial fibrosis?
Effect estimate: β -0.1272
p-value: p=0.0002
This Mendelian randomization study provides evidence for a causal relationship between specific gut microbiota and myocardial interstitial fibrosis, partially mediated by plasma sphingomyelin.
Faecalibacterium may reduce interstitial fibrosis via sphingomyelin; hypothesis-generating for microbiome interventions, needs prospective trials.
BACKGROUND: Prior studies established associations between gut microbiota and myocardial interstitial fibrosis. Nevertheless, the causal relationships and potential intermediaries remain unknown. Thus, we employed a Mendelian randomization strategy to explore whether gut microbiota causally influence myocardial interstitial fibrosis and to assess whether plasma metabolites serve as potential intermediaries in this pathway. METHODS: A two-sample Mendelian randomization approach was performed, utilizing genome-wide association studies to examine the causal relationship between gut microbiota (n= 18,340) and myocardial interstitial fibrosis (n=41,505). Additionally, an investigation was conducted to determine the potential mediation by four plasma metabolites (n=8,299) via a two-step Mendelian randomization analysis. Inverse variance weighted method was the primary method employed in Mendelian randomization, and complementary analyses were conducted alongside to enhance the robustness of the results. RESULTS: Mendelian randomization analysis indicated suggestive associations of three microbial taxa with myocardial interstitial fibrosis. The most significant taxon was the genus Faecalibacterium (β [SE], -0.1272 [0.0347], P = 0.0002). Reverse Mendelian randomization analyses revealed no evidence of myocardial interstitial fibrosis affecting these three microbial taxa. In the two-step Mendelian randomization analysis involving four plasma metabolites, it was found that plasma sphingomyelin levels mediated the causal effects of genus Faecalibacterium on myocardial interstitial fibrosis (proportion mediated = 14.2%, 95% CI = 1.4-27.0%). CONCLUSION: The study validates the causality between particular gut microbial taxa and myocardial interstitial fibrosis, and suggests that plasma sphingomyelin might mediate this association. These findings offer a novel perspective on myocardial interstitial fibrosis prevention, and underscore the significance of plasma sphingomyelin in human health and disease.
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Yu et al. (2025) conducted an observational in Myocardial interstitial fibrosis (n=41,505). Gut microbiota (genus Faecalibacterium) was evaluated on Myocardial interstitial fibrosis (β -0.1272, p=0.0002). Genetically predicted abundance of the genus Faecalibacterium was causally associated with reduced myocardial interstitial fibrosis (β -0.1272, P=0.0002), mediated by plasma sphingomyelin (14.2%).
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