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- W3117688753 abstract "There is a high level of interest in identifying metabolites of endogenously produced or dietary compounds generated by the gastrointestinal (GI) tract microbiota, and determining the functions of these metabolites in health and disease. There is a wealth of compelling evidence that the microbiota is linked with many complex chronic inflammatory diseases, including atherosclerosis. Macrophages are key target immune cells in atherosclerosis. A hallmark of atherosclerosis is the accumulation of pro-inflammatory macrophages in coronary arteries that respond to pro-atherogenic stimuli and failure of digesting lipids that contribute to foam cell formation in atherosclerotic plaques. This review illustrates the role of tryptophan-derived microbiota metabolites as an aryl hydrocarbon receptor (AhR) ligand that has immunomodulatory properties. Also, microbiota-dependent trimethylamine-N-oxide (TMAO) metabolite production is associated with a deleterious effect that promotes atherosclerosis, and metabolite indoxyl sulfate has been shown to exacerbate atherosclerosis. Our objective in this review is to discuss the role of microbiota-derived metabolites in atherosclerosis, specifically the consequences of microbiota-induced effects of innate immunity in response to atherogenic stimuli, and how specific beneficial/detrimental metabolites impact the development of atherosclerosis by regulating chronic endotoxemic and lipotoxic inflammation." @default.
- W3117688753 created "2021-01-05" @default.
- W3117688753 creator A5003846107 @default.
- W3117688753 creator A5032197289 @default.
- W3117688753 creator A5032989116 @default.
- W3117688753 creator A5080653951 @default.
- W3117688753 date "2021-01-01" @default.
- W3117688753 modified "2023-10-16" @default.
- W3117688753 title "Microbiota-Mediated Immune Regulation in Atherosclerosis" @default.
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- W3117688753 doi "https://doi.org/10.3390/molecules26010179" @default.
- W3117688753 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7795654" @default.
- W3117688753 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/33401401" @default.
- W3117688753 hasPublicationYear "2021" @default.
- W3117688753 type Work @default.