The origin of trimethylamine-N-oxide (TMAO) and its role in development of atherosclerosis
Cardiovascular disease (CVD) is a leading cause of deaths and is a growing epidemic worldwide. Atherosclerosis, the primary cause of heart diseases and stroke, is associated with vascular inflammation and accumulation of lipids and fibrous elements in the arteries. Recently, blood trimethylamine-N-oxide (TMAO) has been identified as an independent risk factor for CVD in humans. TMAO is mainly derived from dietary trimethylamine (TMA)-containing nutrients via the bioconversion of gut microbiota and hepatic flavin monooxygenases (FMOs). Both in vivo and in vitro studies have revealed that TMAO promotes atherogenesis by exacerbating vascular inflammation, impairing vascular functions and disturbing cholesterol homeostasis at multiple levels. This review summarizes the current research on the microbiota-dependent generation pathway of TMAO, the associations of TMAO with atherosclerosis, and the potential dietary interventions to reduce the TMAO-associated risk of CVD.
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