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Abstract
Microbial cutC-dependent production of trimethylamine (TMA) is sufficient to enhance platelet reactivity and thrombosis potential in mice.
- Gut microbes produce trimethylamine N-oxide (TMAO), which is linked to cardiovascular disease and thrombosis risks.
- The generation of TMA, a precursor to TMAO, is regulated by choline TMA-lyases encoded by cutC/D genes in human gut bacteria.
- Gnotobiotic mice studies demonstrate that microbial cutC gene expression leads to increased TMA production.
- Heightened platelet reactivity and thrombosis potential were observed in mice colonized with TMA-producing human fecal communities.
- Targeting the microbial choline TMA-lyase pathway may offer a new approach for treating atherothrombotic heart disease.
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