Intestinal bacteria produce metabolites such as trimethylamine N-oxide (TMAO), which have been found to impact the pathological process of coronary artery atherosclerotic disease through various signaling pathways. TMAO has been shown to induce vascular endothelial cell damage, contribute to lipid deposition in the vascular wall, promote inflammation, and stimulate smooth muscle cell aging and migration. Research suggests that modulation of TMAO metabolism and associated signaling pathways may offer potential therapeutic interventions for the prevention and treatment of atherosclerotic disease. This article will provide a brief overview of the TMAO mechanism in atherosclerosis, offering new research insights for the prevention and treatment of this disease.