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Contribution of trimethylamine N-oxide (TMAO) to chronic inflammatory and degenerative diseases

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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

Among Europeans, the GG genotype has been observed to significantly elevate the likelihood of developing TED