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[Research progress of trimethylamine-N-oxide in the pathogenesis of atherosclerosis].
- Source :
-
Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences [Zhong Nan Da Xue Xue Bao Yi Xue Ban] 2017 Aug 28; Vol. 42 (8), pp. 986-990. - Publication Year :
- 2017
-
Abstract
- Trimethylamine-N-oxide (TMAO), metabolites of the intestinal microflora, is a newly discovered risk factor for cardiovascular disease. The intestinal flora converted choline and L-carnitine into trimethylamine in the food. Trimethylamine is oxidized to TMAO in liver enzymes. Lowering TMA can stimulate macrophages to reverse cholesterol transport and inhibit atherogenesis. TMAO poietin-monooxygenase 3 (FMO3) is a tool for cholesterol metabolism and reverse cholesterol transpor, lowering FMO3 can slow the gallbladder's secretion of bile, delay intestinal absorption of cholesterol, and limit the synthesis of oxidized cholesterol and cholesterol esters. TMAO in the blood can up regulate scavenger receptors in macrophages, and promote accumulation of cholesterol and formation of foam cells in macrophages, thereby promoting vascular plaque formation and promote the inflammatory response by MAPK and nuclear factor kappa B pathway. TMAO concentrates on affecting cholesterol metabolism, increasing insulin resistance, promoting platelet aggregation, increasing thrombosis, promoting vascular inflammatory response and directly leading to the formation of atherosclerotic plaques. Lowering TMAO levels can potentially prevent or treat atherosclerotic related diseases and reduce the incidence of cardiovascular and cerebrovascular diseases.
- Subjects :
- Humans
Methylamines
Oxides
Atherosclerosis
Subjects
Details
- Language :
- Chinese
- ISSN :
- 1672-7347
- Volume :
- 42
- Issue :
- 8
- Database :
- MEDLINE
- Journal :
- Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences
- Publication Type :
- Academic Journal
- Accession number :
- 28872093
- Full Text :
- https://doi.org/10.11817/j.issn.1672-7347.2017.08.018