2020
DOI: 10.1111/apm.13038
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Gut microbiota in atherosclerosis: focus on trimethylamine N‐oxide

Abstract: in atherosclerosis: focus on trimethylamine N-oxide. APMIS 2020; 128: 353-366.The increasing prevalence of cardiovascular diseases cannot adequately be explained by traditional risk factors. Recently, accumulating evidence has suggested that gut microbiota-derived numerous metabolites are contributors to atherosclerotic events. Among them, the role of trimethylamine N-oxide (TMAO) in promoting atherosclerosis has gained attention. TMAO is reported to exert the proatherogenic effects by impacting on the traditi… Show more

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Cited by 101 publications
(64 citation statements)
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References 119 publications
(159 reference statements)
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“…Methylglyoxal is a product of glucose and glycine metabolism that increases the activity of the gut microbial trimethylamine (TMA)-lyase [ 46 ]. TMA lyase catalyzes the transformation of dietary choline and carnitine to TMA, which in turn is metabolized by the liver to trimethylamine-N-oxide (TMAO), a potential risk factor for cardiovascular diseases [ 47 ]. The pan-genome of the Liebefeld selection covers the superpathway “methylglyoxal degradation IV” similarly to subjects MH0002 and MH0003.…”
Section: Resultsmentioning
confidence: 99%
“…Methylglyoxal is a product of glucose and glycine metabolism that increases the activity of the gut microbial trimethylamine (TMA)-lyase [ 46 ]. TMA lyase catalyzes the transformation of dietary choline and carnitine to TMA, which in turn is metabolized by the liver to trimethylamine-N-oxide (TMAO), a potential risk factor for cardiovascular diseases [ 47 ]. The pan-genome of the Liebefeld selection covers the superpathway “methylglyoxal degradation IV” similarly to subjects MH0002 and MH0003.…”
Section: Resultsmentioning
confidence: 99%
“…A significant hallmark of atherosclerosis is the accumulation of pro-inflammatory Macs and dendritic cells (DCs) in coronary arteries that respond to pro-atherogenic stimuli, such as free fatty acids (FFAs) and oxidized LDLs (oxLDLs), and the failure to digest lipids that contribute to the formation of foam cells in atherosclerotic plaques [ 16 , 17 ]. Mechanisms that reduce Mac/DC inflammation, increase lipid degradation, and prevent foam cell formation would all decrease atherosclerosis progression.…”
Section: Microbiota-derived Metabolites Associated With Atherosclementioning
confidence: 99%
“…TMA is a metabolic precursor that is converted to a trimethylamine N-oxide (TMAO) in the liver. TMAO drives atherosclerosis progression [110], in part, by regulating macrophage activation and foam cell formation, platelet activation, and aggregation, resulting in elevated expression of IL-1β, IL-6, and TNFα inflammatory cytokines [134]. Recent work implies that TMAO could be also involved in metabolic dysfunction and activation of inflammation, directly acting via its receptor protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) [135].…”
Section: Intestinal Microbiota In Cvd Developmentmentioning
confidence: 99%