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The main cause of death in patients with end-stage renal disease (ESRD) is cardiovascular disease, and trimethylamine-N-oxide (TMAO) has been found to be one of the specific risk factors in the pathogenic process in recent years. TMAO is derived from intestinal bacterial metabolism of dietary choline, carnitine and other substances and subsequently catalyzed by flavin monooxygenase enzymes in the liver. The changes of intestinal bacteria in ESRD patients have contributed to the accumulation of gut-derived uremic toxins such as TMAO, indoxyl sulfate and indole-3-acetic acid. While elevated TMAO concentration accelerates atherosclerosis through mechanisms such as inflammation, increased scavenger receptor expression, and inhibition of reverse cholesterol transport. In this review, this research introduces the biological function, metabolic processes of TMAO and mechanisms by which TMAO promotes the progression of cardiovascular disease in ESRD patients and summarizes current interventions that may be used to reverse gut microbiota disturbances, such as activated carbon, fecal microbial transplantation, dietary improvement, probiotic and probiotic introduction. It also focuses on exploring intervention targets to reduce the gut-derived uremic toxin TMAO in order to explore the possibility of more cardiovascular disease treatments for ESRD patients.终末期肾脏病（ESRD）患者的主要死因是心血管疾病，近年来发现三甲胺-N-氧化物（TMAO）是致病过程中的特异性危险因素之一。TMAO由膳食中胆碱、肉碱等物质经肠道微生物代谢、肝脏黄素单加氧酶催化生成。ESRD患者的肠道菌群改变，促使肠源性尿毒症毒素（TMAO、吲哚硫酸盐、吲哚-3-乙酸等）蓄积，而升高的TMAO通过促炎、增加清道夫受体表达、抑制胆固醇逆向转运等机制加速动脉粥样硬化。在这篇综述中，本研究介绍了TMAO的生理功能、代谢过程及ESRD中TMAO促进心血管疾病发生与发展的机制，回顾了目前可能用于逆转肠道微生物群紊乱的干预措施，如活性炭制剂、粪便微生物移植、膳食改善、益生元和益生菌引入，并重点探究降低肠源性尿毒症毒素TMAO的干预靶点，旨在为ESRD患者探寻更多心血管疾病治疗的可能性。. |
