The gut microbial metabolite trimethylamine N-oxide and cardiovascular diseases

Morbidity and mortality of cardiovascular diseases (CVDs) are exceedingly high worldwide. Researchers have found that the occurrence and development of CVDs are closely related to intestinal microecology. Imbalances in intestinal microecology caused by changes in the composition of the intestinal microbiota will eventually alter intestinal metabolites, thus transforming the host physiological state from healthy mode to pathological mode. Trimethylamine N-oxide (TMAO) is produced from the metabolism of dietary choline and L-carnitine by intestinal microbiota, and many studies have shown that this important product inhibits cholesterol metabolism, induces platelet aggregation and thrombosis, and promotes atherosclerosis. TMAO is directly or indirectly involved in the pathogenesis of CVDs and is an important risk factor affecting the occurrence and even prognosis of CVDs. This review presents the biological and chemical characteristics of TMAO, and the process of TMAO produced by gut microbiota. In particular, the review focuses on summarizing how the increase of gut microbial metabolite TMAO affects CVDs including atherosclerosis, heart failure, hypertension, arrhythmia, coronary artery disease, and other CVD-related diseases. Understanding the mechanism of how increases in TMAO promotes CVDs will potentially facilitate the identification and development of targeted therapy for CVDs.

Automated summary

Cardiovascular diseases (CVDs) are highly prevalent worldwide, and the balance of intestinal microecology plays a crucial role in their occurrence and development. Trimethylamine N-oxide (TMAO), a metabolite produced by gut microbiota from dietary choline and L-carnitine, has been found to inhibit cholesterol metabolism, induce platelet aggregation, and promote atherosclerosis. This review provides insights into the biological and chemical characteristics of TMAO, as well as its impact on various CVDs, including atherosclerosis, heart failure, hypertension, arrhythmia, and coronary artery disease. Understanding the mechanism of TMAO in promoting CVDs may contribute to the development of targeted therapies.