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...
Gespeichert in:
Veröffentlicht in: | Heart (British Cardiac Society) 2022-06, Vol.108 (12), p.917-922 |
---|---|
Hauptverfasser: | , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 922 |
---|---|
container_issue | 12 |
container_start_page | 917 |
container_title | Heart (British Cardiac Society) |
container_volume | 108 |
creator | Lv, Shichao 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 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2579633855</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2671680103</sourcerecordid><originalsourceid>FETCH-LOGICAL-b376t-9e50ce1817c3b6e4f59a03116bec8c5d814379137807c120828be775885d38d23</originalsourceid><addsrcrecordid>eNp9kE1Lw0AQhhdRrFb_gUjAi5foTDb7EW9a_IKClwrelk0ysSn5qJsN2H9valsFD55mGJ55Z3gYO0O4QuTyek7W-UVThRFEGPIIQMR77AhjqYcRvu0PPRcilMDViB133QIA4kTLQzbisUSEWB2xu5kra_LzVWXrsqGg_SxzuglssGw9Nb60VeCteycfFK0Lvm8GhS2r3lHg5-TscnXCDgpbdXS6rWP2-nA_mzyF05fH58ntNEy5kj5MSEBGqFFlPJUUFyKxwBFlSpnORK4x5ipBrjSoDCPQkU5JKaG1yLnOIz5ml5vcpWs_euq8qcsuo6qyDbV9ZyKhEsm5FmJAL_6gi7Z3zfCdiaRCqQGBD1S8oTLXdp2jwiwHGdatDIJZOzY7x2bt2GwcD2vn2_A-rSn_WdpJHQDYAGm9-D38b-YXBKaHVA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2671680103</pqid></control><display><type>article</type><title>Trimethylamine oxide: a potential target for heart failure therapy</title><source>MEDLINE</source><source>PubMed Central</source><creator>Lv, Shichao ; Wang, Yunjiao ; Zhang, Wanqin ; Shang, Hongcai</creator><creatorcontrib>Lv, Shichao ; Wang, Yunjiao ; Zhang, Wanqin ; Shang, Hongcai</creatorcontrib><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.</description><identifier>ISSN: 1355-6037</identifier><identifier>EISSN: 1468-201X</identifier><identifier>DOI: 10.1136/heartjnl-2021-320054</identifier><identifier>PMID: 34611047</identifier><language>eng</language><publisher>England: BMJ Publishing Group Ltd and British Cardiovascular Society</publisher><subject>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</subject><ispartof>Heart (British Cardiac Society), 2022-06, Vol.108 (12), p.917-922</ispartof><rights>Author(s) (or their employer(s)) 2022. No commercial re-use. See rights and permissions. Published by BMJ.</rights><rights>2022 Author(s) (or their employer(s)) 2022. No commercial re-use. See rights and permissions. Published by BMJ.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b376t-9e50ce1817c3b6e4f59a03116bec8c5d814379137807c120828be775885d38d23</citedby><cites>FETCH-LOGICAL-b376t-9e50ce1817c3b6e4f59a03116bec8c5d814379137807c120828be775885d38d23</cites><orcidid>0000-0002-4073-9083</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34611047$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lv, Shichao</creatorcontrib><creatorcontrib>Wang, Yunjiao</creatorcontrib><creatorcontrib>Zhang, Wanqin</creatorcontrib><creatorcontrib>Shang, Hongcai</creatorcontrib><title>Trimethylamine oxide: a potential target for heart failure therapy</title><title>Heart (British Cardiac Society)</title><addtitle>Heart</addtitle><addtitle>Heart</addtitle><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.</description><subject>Campylobacter</subject><subject>Cardiac function</subject><subject>Cardiotonic Agents</subject><subject>Cardiovascular disease</subject><subject>Carnitine - metabolism</subject><subject>Choline - metabolism</subject><subject>Cytokines</subject><subject>Diabetes</subject><subject>Diuretics</subject><subject>Edema</subject><subject>Ejection fraction</subject><subject>Gastrointestinal Microbiome - physiology</subject><subject>Health care</subject><subject>Heart failure</subject><subject>Heart Failure - drug therapy</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>inflammation</subject><subject>Ischemia</subject><subject>Medical prognosis</subject><subject>Methylamines</subject><subject>Microbiota</subject><subject>Morbidity</subject><subject>Mortality</subject><subject>Permeability</subject><subject>Review</subject><subject>Salmonella</subject><subject>Tumor necrosis factor-TNF</subject><issn>1355-6037</issn><issn>1468-201X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kE1Lw0AQhhdRrFb_gUjAi5foTDb7EW9a_IKClwrelk0ysSn5qJsN2H9valsFD55mGJ55Z3gYO0O4QuTyek7W-UVThRFEGPIIQMR77AhjqYcRvu0PPRcilMDViB133QIA4kTLQzbisUSEWB2xu5kra_LzVWXrsqGg_SxzuglssGw9Nb60VeCteycfFK0Lvm8GhS2r3lHg5-TscnXCDgpbdXS6rWP2-nA_mzyF05fH58ntNEy5kj5MSEBGqFFlPJUUFyKxwBFlSpnORK4x5ipBrjSoDCPQkU5JKaG1yLnOIz5ml5vcpWs_euq8qcsuo6qyDbV9ZyKhEsm5FmJAL_6gi7Z3zfCdiaRCqQGBD1S8oTLXdp2jwiwHGdatDIJZOzY7x2bt2GwcD2vn2_A-rSn_WdpJHQDYAGm9-D38b-YXBKaHVA</recordid><startdate>20220601</startdate><enddate>20220601</enddate><creator>Lv, Shichao</creator><creator>Wang, Yunjiao</creator><creator>Zhang, Wanqin</creator><creator>Shang, Hongcai</creator><general>BMJ Publishing Group Ltd and British Cardiovascular Society</general><general>BMJ Publishing Group LTD</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4073-9083</orcidid></search><sort><creationdate>20220601</creationdate><title>Trimethylamine oxide: a potential target for heart failure therapy</title><author>Lv, Shichao ; Wang, Yunjiao ; Zhang, Wanqin ; Shang, Hongcai</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b376t-9e50ce1817c3b6e4f59a03116bec8c5d814379137807c120828be775885d38d23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Campylobacter</topic><topic>Cardiac function</topic><topic>Cardiotonic Agents</topic><topic>Cardiovascular disease</topic><topic>Carnitine - metabolism</topic><topic>Choline - metabolism</topic><topic>Cytokines</topic><topic>Diabetes</topic><topic>Diuretics</topic><topic>Edema</topic><topic>Ejection fraction</topic><topic>Gastrointestinal Microbiome - physiology</topic><topic>Health care</topic><topic>Heart failure</topic><topic>Heart Failure - drug therapy</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>inflammation</topic><topic>Ischemia</topic><topic>Medical prognosis</topic><topic>Methylamines</topic><topic>Microbiota</topic><topic>Morbidity</topic><topic>Mortality</topic><topic>Permeability</topic><topic>Review</topic><topic>Salmonella</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lv, Shichao</creatorcontrib><creatorcontrib>Wang, Yunjiao</creatorcontrib><creatorcontrib>Zhang, Wanqin</creatorcontrib><creatorcontrib>Shang, Hongcai</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Heart (British Cardiac Society)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lv, Shichao</au><au>Wang, Yunjiao</au><au>Zhang, Wanqin</au><au>Shang, Hongcai</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Trimethylamine oxide: a potential target for heart failure therapy</atitle><jtitle>Heart (British Cardiac Society)</jtitle><stitle>Heart</stitle><addtitle>Heart</addtitle><date>2022-06-01</date><risdate>2022</risdate><volume>108</volume><issue>12</issue><spage>917</spage><epage>922</epage><pages>917-922</pages><issn>1355-6037</issn><eissn>1468-201X</eissn><abstract>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.</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> |
fulltext | fulltext |
identifier | ISSN: 1355-6037 |
ispartof | Heart (British Cardiac Society), 2022-06, Vol.108 (12), p.917-922 |
issn | 1355-6037 1468-201X |
language | eng |
recordid | cdi_proquest_miscellaneous_2579633855 |
source | MEDLINE; PubMed Central |
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 |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T15%3A45%3A03IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Trimethylamine%20oxide:%20a%20potential%20target%20for%20heart%20failure%20therapy&rft.jtitle=Heart%20(British%20Cardiac%20Society)&rft.au=Lv,%20Shichao&rft.date=2022-06-01&rft.volume=108&rft.issue=12&rft.spage=917&rft.epage=922&rft.pages=917-922&rft.issn=1355-6037&rft.eissn=1468-201X&rft_id=info:doi/10.1136/heartjnl-2021-320054&rft_dat=%3Cproquest_cross%3E2671680103%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2671680103&rft_id=info:pmid/34611047&rfr_iscdi=true |