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Trimethylamine-N-Oxide promotes vascular calcification through activation of NLRP3 (Nucleotide-Binding domain, leucine-rich-containing family, pyrin domain-containing-3) inflammasome and NF-B (nuclear factor B) signals

In mice with intact gut microbiota, dietary supplementation of TMAO, carnitine, or high choline can significantly reduce the reverse transport of cholesterol in the body, thereby aggravating the progression of atherosclerosis in mice ( / mice expressing human cholesteryl ester transfer protein (hCETP), TMAO derived from L-carnitine levels inversely correlated with aortic lesion size in both the aortic root and thoracic aorta ( The Molecular Mechanism of TMAO Aggravating Coronary Atherosclerosis Vascular Dysfunction: TMAO Promotes Oxidative Stress and Inflammation in Endothelial Cells Vascular dysfunction is an important risk factor for atherosclerotic heart disease (Figure 2) has shown that TMAO can activate the inflammasome NOD-like receptor protein 3 (Nlrp3) through different pathways to activate the inflammatory signal pathway, resulting in aggravation of oxidative stress and, in turn, of endothelial dysfunction

Use with caution in pregnant or breastfeeding women, as safety data in these populations are limited

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Effect of externally added carnitine on the synthesis of acetylcholine in rat cerebral cortex cells

The potential of TMAO to result in atherogenic effects is linked to alterations in cholesterol and bile acid metabolism, inflammatory pathway activation, and foam cell formation promotion