Morbidity and mortality of cardiovascular diseases (CVDs) are exceedingly high worldwide. Researchers have found that the occurrence and development of CVDs are closely related to intestinal microecology. Imbalances in intestinal microecology caused by changes in the composition of the intestinal microbiota will eventually alter intestinal metabolites, thus transforming the host physiological state from healthy mode to pathological mode. Trimethylamine N-oxide (TMAO) is produced from the metabolism of dietary choline and L-carnitine by intestinal microbiota, and many studies have shown that this important product inhibits cholesterol metabolism, induces platelet aggregation and thrombosis, and promotes atherosclerosis. TMAO is directly or indirectly involved in the pathogenesis of CVDs and is an important risk factor affecting the occurrence and even prognosis of CVDs. This review presents the biological and chemical characteristics of TMAO, and the process of TMAO produced by gut microbiota. In particular, the review focuses on summarizing how the increase of gut microbial metabolite TMAO affects CVDs including atherosclerosis, heart failure, hypertension, arrhythmia, coronary artery disease, and other CVD-related diseases. Understanding the mechanism of how increases in TMAO promotes CVDs will potentially facilitate the identification and development of targeted therapy for CVDs.

中文翻译：

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肠道微生物代谢产物三甲胺N-氧化物与心血管疾病

全世界心血管疾病 (CVD) 的发病率和死亡率都非常高。研究人员发现，心血管疾病的发生、发展与肠道微生态密切相关。肠道菌群组成变化引起的肠道微生态失衡最终会改变肠道代谢产物，从而使宿主生理状态从健康模式转变为病理模式。三甲胺N-氧化物（TMAO）是由肠道微生物群代谢膳食胆碱和左旋肉碱产生的，许多研究表明，这种重要产物抑制胆固醇代谢，诱导血小板聚集和血栓形成，促进动脉粥样硬化。TMAO直接或间接参与CVD的发病，是影响CVD发生乃至预后的重要危险因素。本综述介绍了 TMAO 的生物学和化学特性，以及肠道微生物群产生 TMAO 的过程。特别是，该综述重点总结了肠道微生物代谢物 TMAO 的增加如何影响 CVD，包括动脉粥样硬化、心力衰竭、高血压、心律失常、冠状动脉疾病和其他 CVD 相关疾病。了解 TMAO 增加如何促进 CVD 的机制将可能促进 CVD 靶向治疗的识别和开发。该综述重点总结了肠道微生物代谢物TMAO的增加如何影响心血管疾病，包括动脉粥样硬化、心力衰竭、高血压、心律失常、冠状动脉疾病和其他心血管疾病相关疾病。了解 TMAO 增加如何促进 CVD 的机制将可能促进 CVD 靶向治疗的识别和开发。该综述重点总结了肠道微生物代谢物TMAO的增加如何影响心血管疾病，包括动脉粥样硬化、心力衰竭、高血压、心律失常、冠状动脉疾病和其他心血管疾病相关疾病。了解 TMAO 增加如何促进 CVD 的机制将可能促进 CVD 靶向治疗的识别和开发。