Jiahuan He, Hanwen Wang, Eric Qiu, Qibin Qi, Zheng Wang
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. 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.