Trimethylamine oxide: a potential target for heart failure therapy

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...

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Veröffentlicht in:Heart (British Cardiac Society) 2022-06, Vol.108 (12), p.917-922
Hauptverfasser: Lv, Shichao, Wang, Yunjiao, Zhang, Wanqin, Shang, Hongcai
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Wang, Yunjiao
Zhang, Wanqin
Shang, Hongcai
description 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.
doi_str_mv 10.1136/heartjnl-2021-320054
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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. 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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. 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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.</abstract><cop>England</cop><pub>BMJ Publishing Group Ltd and British Cardiovascular Society</pub><pmid>34611047</pmid><doi>10.1136/heartjnl-2021-320054</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0002-4073-9083</orcidid></addata></record>
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subjects Campylobacter
Cardiac function
Cardiotonic Agents
Cardiovascular disease
Carnitine - metabolism
Choline - metabolism
Cytokines
Diabetes
Diuretics
Edema
Ejection fraction
Gastrointestinal Microbiome - physiology
Health care
Heart failure
Heart Failure - drug therapy
Homeostasis
Humans
inflammation
Ischemia
Medical prognosis
Methylamines
Microbiota
Morbidity
Mortality
Permeability
Review
Salmonella
Tumor necrosis factor-TNF
title Trimethylamine oxide: a potential target for heart failure therapy
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