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Trimethylamine oxide: a potential target for heart failure therapy
  1. Shichao Lv1,2,
  2. Yunjiao Wang2,
  3. Wanqin Zhang2,
  4. Hongcai Shang1
  1. 1 Key Laboratory of Chinese Internal Medicine of MOE, Dongzhimen Hospital, BUCM, Beijing, China
  2. 2 First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China
  1. Correspondence to Professor Hongcai Shang, Key Laboratory of Chinese Internal Medicine of MOE, Dongzhimen Hospital, BUCM, Beijing 100700, China; shanghongcai{at}


Heart failure (HF) is a clinical syndrome in the late stage of cardiovascular disease and is associated with high prevalence, mortality and rehospitalisation rate. The pathophysiological mechanisms of HF have experienced the initial ‘water-sodium retention’ mode to ‘abnormal hemodynamics’ mode, and subsequent to ‘abnormal activation of neuroendocrine’ mode, which has extensively promoted the reform of HF treatment and updated the treatment concept. Since the Human Microbiome Project commencement, the study on intestinal microecology has swiftly developed, providing a new direction to reveal the occurrence of diseases and the mechanisms behind drug effects. Intestinal microecology comprises the gastrointestinal lumen, epithelial secretion, food entering the intestine, intestinal flora and metabolites. Choline and L-carnitine in the diet are metabolised to trimethylamine (TMA) by the intestinal micro-organisms, with TMA being absorbed into the blood. TMA then enters the liver through the portal vein circulation and is oxidised to trimethylamine oxide (TMAO) by the hepatic flavin-containing mono-oxygenase (FMO) family, especially FMO3. The circulating TMAO levels are associated with adverse outcomes in HF (mortality and readmission), and lower TMAO levels indicate better prognosis. As HF progresses, the concentration of TMAO in patients gradually increases. Whether the circulating TMAO level can be decreased by intervening with the intestinal microflora or relevant enzymes, thereby affecting the prognosis of patients with HF, has become a research hotspot. Therefore, based on the HF intestinal hypothesis, exploring the treatment strategy for HF targeting the TMAO metabolite of the intestinal flora may update the treatment concept in HF and improve its therapeutic effect.

  • heart failure
  • inflammation

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  • Contributors All authors contributed to the drafting of the manuscript and approved the final content.

  • Funding This work was supported by the National Key R&D Program of China (2017YFC1700400) and the Tianjin Health and Family Planning Industry High-Level Personnel Selection and Training Project.

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Provenance and peer review Not commissioned; externally peer reviewed.