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Purpose of Review <p>This review synthesizes and discusses evidence from metagenomics, metabolomics, and proteomics on gut microbiome alterations in atherosclerotic cardiovascular disease (ACVD), with carotid atherosclerosis (CAS) serving as an example.</p> Recent Findings <p>Evidence on gut microbial α-diversity and β-diversity was mixed and differs by disease status. Pro-inflammatory/pathogenic gut bacterial taxa (e.g., <i>Escherichia coli</i>, <i>Klebsiella spp.</i>, <i>Streptococcus spp.</i>, and <i>Ruminococcus gnavus</i>) were often enriched in patients with ACVD or CAS, whereas short-chain fatty acid (SCFA) producers (e.g., <i>Faecalibacterium prausnitzii</i>, <i>Roseburia spp.</i>, <i>Bacteroides spp.</i>, and <i>Eubacterium eligens</i>) were depleted. Targeted and untargeted metabolomics implicated multiple microbial-derived metabolites in relation to ACVD and CAS, including trimethylamine N-oxide, short-chain fatty acids, bile acids, lipopolysaccharides, phenylacetylglutamine, indole-3-propionate and imidazole propionate.</p> Summary <p>Gut dysbiosis contributes to ACVD or CAS possibly via metabolite-mediated effects on endothelial function, inflammation, and lipid metabolism. Future research prioritizing longitudinal and interventional studies integrating microbial metagenomics with host multi-omics are needed to elucidate causal pathways and identify clinically actionable targets.</p>

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Gut Microbiota and Atherosclerosis: Integrative Multi-Omics and Mechanistic Insights

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月18日

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  • Jiahuan Helen He,
  • Hanwen Wang,
  • Eric Qiu,
  • Qibin Qi,
  • Zheng Wang

摘要

Purpose of Review

This review synthesizes and discusses evidence from metagenomics, metabolomics, and proteomics on gut microbiome alterations in atherosclerotic cardiovascular disease (ACVD), with carotid atherosclerosis (CAS) serving as an example.

Recent Findings

Evidence on gut microbial α-diversity and β-diversity was mixed and differs by disease status. Pro-inflammatory/pathogenic gut bacterial taxa (e.g., Escherichia coli, Klebsiella spp., Streptococcus spp., and Ruminococcus gnavus) were often enriched in patients with ACVD or CAS, whereas short-chain fatty acid (SCFA) producers (e.g., Faecalibacterium prausnitzii, Roseburia spp., Bacteroides spp., and Eubacterium eligens) were depleted. Targeted and untargeted metabolomics implicated multiple microbial-derived metabolites in relation to ACVD and CAS, including trimethylamine N-oxide, short-chain fatty acids, bile acids, lipopolysaccharides, phenylacetylglutamine, indole-3-propionate and imidazole propionate.

Summary

Gut dysbiosis contributes to ACVD or CAS possibly via metabolite-mediated effects on endothelial function, inflammation, and lipid metabolism. Future research prioritizing longitudinal and interventional studies integrating microbial metagenomics with host multi-omics are needed to elucidate causal pathways and identify clinically actionable targets.