Two new studies take significant steps toward interventions to reduce cardiac risk in humans by reducing levels of the metabolite TMAO through diet manipulation or targeted therapies.
Findings from a mouse model provide support for a new drug class that acts on gut microbes to reduce platelet responsiveness and thrombosis risk without promoting bleeding or antibiotic resistance.
The gut microbe-dependent metabolite TMAO has been linked to increased near-term cardiac events and increased long-term mortality in patients with acute coronary syndrome. Dr. Stan Hazen explains the study.
A cohort study has tied the gut microbial metabolite TMAO to elevated five-year mortality in patients with peripheral artery disease (PAD). Here’s how treatment targeting in PAD may be shaped in response.
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Yet another cardiometabolic effect has been linked to the gut microbial metabolite TMAO: increased thrombotic risk stemming from platelet hyperreactivity. The lead Cleveland Clinic researcher discusses the implications.
The story linking gut microbes, TMAO and heart disease has turned toward therapy interventions with the first demonstrated targeting of a gut microbial pathway to curb diet-induced heart disease.