Fig. 1

Some intestinal metabolites promote the development of atherosclerosis. Choline in food is transformed into trimethylamine by the action of intestinal bacteria, and the latter is formed into TMAO by the action of a specific group of bacteria containing the CutC gene. TMAO evokes the release of intracellular calcium stores and promotes platelet activation and atherosclerotic plaque formation. Phenylalanine in food is converted to phenylacetic acid by the action of porA gene-containing enteric flora, which synthesizes PAGln or PAGly with glutamine or glycine and binds to platelet adrenergic receptors to induce platelet hyperreactivity and promote atherogenic plaque formation