Life sciencesSep 23, 2025

Gut bacteria imbalance and their products linked to heart disease and treatment

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Jan 2, 2026

Abstract

Gut microbiome dysbiosis is implicated in diverse cardiovascular diseases (CVDs), including hypertension and heart failure.

Microbial-derived metabolites, such as trimethylamine N-oxide (TMAO) and short-chain fatty acids (SCFAs), may influence cardiovascular health.
TMAO is linked to plaque instability, while SCFAs are associated with regulating blood pressure and endothelial function.
Other metabolites, like phenylacetylglutamine (PAGln) and bile acids, could promote thrombotic pathways and affect lipid metabolism, respectively.
Emerging strategies to modulate the gut microbiota may involve precision probiotics, dietary changes, and pharmacological interventions.
Challenges in understanding causal pathways and standardizing interventions across populations remain significant.
Future research is needed to conduct longitudinal studies and randomized trials to explore the potential of gut microbiota in CVD prevention.

Simplified

The gut microbiota, a dynamic ecosystem of microorganisms inhabiting the human body, plays a pivotal role in modulating host physiology and immune function, with intense implications for the cardiovascular system. Cardiovascular diseases (CVDs) stand out as the leading cause of mortality worldwide. Gut microbiome dysbiosis is implicated in diverse CVDs, such as hypertension, atherosclerosis, coronary artery disease, heart failure, and myocardial infarction, through mechanisms mediated by microbial-derived metabolites. Key compounds include trimethylamine N-oxide (TMAO) (linked to plaque instability), short-chain fatty acids (SCFAs) (which regulate blood pressure and endothelial function), phenylacetylglutamine (PAGln) (a promoter of thrombotic pathways), and bile acids (influencing lipid metabolism). These metabolites serve as both biomarkers of CVD risk and therapeutic targets. Emerging strategies to modulate the gut microbiota, such as precision probiotics, dietary interventions (e.g., fiber-rich or polyphenol-heavy diets), and pharmacologic inhibitors of microbial enzymes (e.g., TMA lyase blockers), highlight the potential for microbiome-directed therapies. However, challenges remain in elucidating causal microbial pathways, standardizing interventions across diverse populations, and translating preclinical findings into clinical practice. In this mechanistic and translational review, we synthesize current evidence on the bidirectional relationship between gut microbial dysbiosis and CVDs. We explore how modifiable factors, including diet, pharmacotherapy, and early-life microbial colonization, reshape gut communities, driving systemic inflammation, metabolic dysfunction, and vascular pathology. Future research must prioritize longitudinal human studies, multi-omics integration, and randomized trials to harness the gut microbiota's full potential in CVD prevention and personalized treatment.

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Declaration of competing interest The authors report no financial or non-financial conflicts of interest.

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Gut bacteria imbalance and their products linked to heart disease and treatment

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