Gut Metabolite Trimethylamine-N-Oxide in Atherosclerosis: From Mechanism to Therapy

Atherosclerosis is associated with various pathological manifestations, such as ischemic heart disease, ischemic stroke, and peripheral arterial disease, and remains a leading cause of public health concern. Atherosclerosis is an inflammatory disease characterized by endothelial dysfunction; vascula...

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Autores principales:	BingYu Wang, Jun Qiu, JiangFang Lian, Xi Yang, JianQing Zhou
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	TMAO L-carnitine atherosclerosis endoplasmic reticulum stress vascular calcification Diseases of the circulatory (Cardiovascular) system RC666-701
Acceso en línea:	https://doaj.org/article/e8a9bb3ab4314e5abc746cabc4336c9e
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spelling	oai:doaj.org-article:e8a9bb3ab4314e5abc746cabc4336c9e2021-11-30T14:29:17ZGut Metabolite Trimethylamine-N-Oxide in Atherosclerosis: From Mechanism to Therapy2297-055X10.3389/fcvm.2021.723886https://doaj.org/article/e8a9bb3ab4314e5abc746cabc4336c9e2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fcvm.2021.723886/fullhttps://doaj.org/toc/2297-055XAtherosclerosis is associated with various pathological manifestations, such as ischemic heart disease, ischemic stroke, and peripheral arterial disease, and remains a leading cause of public health concern. Atherosclerosis is an inflammatory disease characterized by endothelial dysfunction; vascular inflammation; and the deposition of lipids, cholesterol, calcium, and cellular debris within the vessel wall intima. In-depth studies of gut flora in recent years have shown that bacterial translocation and the existence of bacterial active products in blood circulation can affect the inflammatory state of the whole blood vessel. The gut flora is considered to be a large “secretory organ,” which produces trimethylamine-N-oxide (TMAO), short-chain fatty acids and secondary bile acids by breaking down the ingested food. Studies have shown that TMAO is an independent risk factor for the occurrence of malignant adverse cardiovascular events, but whether it is harmful or beneficial to patients with cardiovascular diseases with mild or no clinical manifestations remains controversial. We review the relationship between TMAO and its precursor (L-carnitine) and coronary atherosclerosis and summarize the potential molecular mechanism and therapeutic measures of TMAO on coronary atherosclerosis.BingYu WangJun QiuJiangFang LianJiangFang LianXi YangJianQing ZhouJianQing ZhouFrontiers Media S.A.articleTMAOL-carnitineatherosclerosisendoplasmic reticulum stressvascular calcificationDiseases of the circulatory (Cardiovascular) systemRC666-701ENFrontiers in Cardiovascular Medicine, Vol 8 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	TMAO L-carnitine atherosclerosis endoplasmic reticulum stress vascular calcification Diseases of the circulatory (Cardiovascular) system RC666-701
spellingShingle	TMAO L-carnitine atherosclerosis endoplasmic reticulum stress vascular calcification Diseases of the circulatory (Cardiovascular) system RC666-701 BingYu Wang Jun Qiu JiangFang Lian JiangFang Lian Xi Yang JianQing Zhou JianQing Zhou Gut Metabolite Trimethylamine-N-Oxide in Atherosclerosis: From Mechanism to Therapy
description	Atherosclerosis is associated with various pathological manifestations, such as ischemic heart disease, ischemic stroke, and peripheral arterial disease, and remains a leading cause of public health concern. Atherosclerosis is an inflammatory disease characterized by endothelial dysfunction; vascular inflammation; and the deposition of lipids, cholesterol, calcium, and cellular debris within the vessel wall intima. In-depth studies of gut flora in recent years have shown that bacterial translocation and the existence of bacterial active products in blood circulation can affect the inflammatory state of the whole blood vessel. The gut flora is considered to be a large “secretory organ,” which produces trimethylamine-N-oxide (TMAO), short-chain fatty acids and secondary bile acids by breaking down the ingested food. Studies have shown that TMAO is an independent risk factor for the occurrence of malignant adverse cardiovascular events, but whether it is harmful or beneficial to patients with cardiovascular diseases with mild or no clinical manifestations remains controversial. We review the relationship between TMAO and its precursor (L-carnitine) and coronary atherosclerosis and summarize the potential molecular mechanism and therapeutic measures of TMAO on coronary atherosclerosis.
format	article
author	BingYu Wang Jun Qiu JiangFang Lian JiangFang Lian Xi Yang JianQing Zhou JianQing Zhou
author_facet	BingYu Wang Jun Qiu JiangFang Lian JiangFang Lian Xi Yang JianQing Zhou JianQing Zhou
author_sort	BingYu Wang
title	Gut Metabolite Trimethylamine-N-Oxide in Atherosclerosis: From Mechanism to Therapy
title_short	Gut Metabolite Trimethylamine-N-Oxide in Atherosclerosis: From Mechanism to Therapy
title_full	Gut Metabolite Trimethylamine-N-Oxide in Atherosclerosis: From Mechanism to Therapy
title_fullStr	Gut Metabolite Trimethylamine-N-Oxide in Atherosclerosis: From Mechanism to Therapy
title_full_unstemmed	Gut Metabolite Trimethylamine-N-Oxide in Atherosclerosis: From Mechanism to Therapy
title_sort	gut metabolite trimethylamine-n-oxide in atherosclerosis: from mechanism to therapy
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/e8a9bb3ab4314e5abc746cabc4336c9e
work_keys_str_mv	AT bingyuwang gutmetabolitetrimethylaminenoxideinatherosclerosisfrommechanismtotherapy AT junqiu gutmetabolitetrimethylaminenoxideinatherosclerosisfrommechanismtotherapy AT jiangfanglian gutmetabolitetrimethylaminenoxideinatherosclerosisfrommechanismtotherapy AT jiangfanglian gutmetabolitetrimethylaminenoxideinatherosclerosisfrommechanismtotherapy AT xiyang gutmetabolitetrimethylaminenoxideinatherosclerosisfrommechanismtotherapy AT jianqingzhou gutmetabolitetrimethylaminenoxideinatherosclerosisfrommechanismtotherapy AT jianqingzhou gutmetabolitetrimethylaminenoxideinatherosclerosisfrommechanismtotherapy
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Gut Metabolite Trimethylamine-N-Oxide in Atherosclerosis: From Mechanism to Therapy

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