Gut microbe-derived metabolite trimethylamine N-oxide induces cardiac hypertrophy and fibrosis
Trimethylamine N-oxide (TMAO), a gut microbe-derived metabolite of dietary choline and other trimethylamine-containing nutrients, has been linked to increased cardiovascular disease risk. It is unknown whether TMAO plays a role in the development of cardiac hypertrophy. Transverse aortic constrictio...
Gespeichert in:
| Veröffentlicht in: | Laboratory investigation 2019-03, Vol.99 (3), p.346-357 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 357 |
|---|---|
| container_issue | 3 |
| container_start_page | 346 |
| container_title | Laboratory investigation |
| container_volume | 99 |
| creator | Li, Zehua Wu, Zhiye Yan, Jianyun Liu, Hailin Liu, Qicai Deng, Yi Ou, Caiwen Chen, Minsheng |
| description | Trimethylamine N-oxide (TMAO), a gut microbe-derived metabolite of dietary choline and other trimethylamine-containing nutrients, has been linked to increased cardiovascular disease risk. It is unknown whether TMAO plays a role in the development of cardiac hypertrophy. Transverse aortic constriction (TAC) was performed to induce cardiac hypertrophy in Sprague-Dawley (SD) rats. We observed that TMAO levels were significantly elevated in SD rats after 6 weeks of TAC, suggesting the potential role of TMAO in regulating cardiac hypertrophy. In cultured cardiomyocytes, TMAO treatment stimulated cardiac hypertrophy, as indicated by increased cell area of cardiomyocytes and expression of hypertrophic markers including atrial natriuretic peptide (ANP) and beta-myosin heavy chain (β-MHC). Additionally, TMAO treatment induced cardiac hypertrophy and cardiac fibrosis in SD rats. Reducing TMAO synthesis by antibiotics (Abs) attenuated TAC-induced cardiac hypertrophy and fibrosis. Furthermore, pharmacological inhibition of Smad3 by SIS3 significantly reduced the expression of ANP and β-MHC, and cardiomyocyte cell size in TMAO-treated group. These data for the first time demonstrate that gut microbe-derived metabolite TMAO induces cardiac hypertrophy and fibrosis involving Smad3 signaling, suggesting that inhibition of gut microbes or generation of TMAO may become a potential target for the prevention and treatment of cardiac hypertrophy. |
| doi_str_mv | 10.1038/s41374-018-0091-y |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2186152570</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0023683722006778</els_id><sourcerecordid>2186152570</sourcerecordid><originalsourceid>FETCH-LOGICAL-c581t-fb1e67581e377528aef3154c9bc35a6ddf33329163c98bd9d23670a600f2893</originalsourceid><addsrcrecordid>eNp9kE1P5SAUholx4r1-_AA3hsQ1eiiF0rgyxnFMzMxiZj2EwqmXm3vbK7TG_nsx9WPnCgjv856ch5BTDhcchL5MJRdVyYBrBlBzNu2RJZcCGAio9skSoBBMaVEtyGFKawBelkoekIUAULrmckn-340D3QYX-waZxxie0dMtDrbpN2FAOsSQX6tpY7ehQ_qb9S_BIw2dHx0m6mz0wTq6mnYYh9jvVhO1nadtaGKfQjomP1q7SXjyfh6Rvz9v_938Yg9_7u5vrh-Yk5oPrG04qipfUVSVLLTFVnBZurpxQlrlfSuEKGquhKt142tfCFWBVQBtoWtxRM7n1l3sn0ZMg1n3Y-zyQFNwrbgsZAU5xedUXjaliK3Z5eVsnAwH8-bTzD5N9mnefJopM2fvzWOzRf9JfAjMgWIOpPzVPWL8Gv1d69UMYVbyHDKUXMDOoQ8R3WB8H76hXwEuPJUC</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2186152570</pqid></control><display><type>article</type><title>Gut microbe-derived metabolite trimethylamine N-oxide induces cardiac hypertrophy and fibrosis</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Li, Zehua ; Wu, Zhiye ; Yan, Jianyun ; Liu, Hailin ; Liu, Qicai ; Deng, Yi ; Ou, Caiwen ; Chen, Minsheng</creator><creatorcontrib>Li, Zehua ; Wu, Zhiye ; Yan, Jianyun ; Liu, Hailin ; Liu, Qicai ; Deng, Yi ; Ou, Caiwen ; Chen, Minsheng</creatorcontrib><description>Trimethylamine N-oxide (TMAO), a gut microbe-derived metabolite of dietary choline and other trimethylamine-containing nutrients, has been linked to increased cardiovascular disease risk. It is unknown whether TMAO plays a role in the development of cardiac hypertrophy. Transverse aortic constriction (TAC) was performed to induce cardiac hypertrophy in Sprague-Dawley (SD) rats. We observed that TMAO levels were significantly elevated in SD rats after 6 weeks of TAC, suggesting the potential role of TMAO in regulating cardiac hypertrophy. In cultured cardiomyocytes, TMAO treatment stimulated cardiac hypertrophy, as indicated by increased cell area of cardiomyocytes and expression of hypertrophic markers including atrial natriuretic peptide (ANP) and beta-myosin heavy chain (β-MHC). Additionally, TMAO treatment induced cardiac hypertrophy and cardiac fibrosis in SD rats. Reducing TMAO synthesis by antibiotics (Abs) attenuated TAC-induced cardiac hypertrophy and fibrosis. Furthermore, pharmacological inhibition of Smad3 by SIS3 significantly reduced the expression of ANP and β-MHC, and cardiomyocyte cell size in TMAO-treated group. These data for the first time demonstrate that gut microbe-derived metabolite TMAO induces cardiac hypertrophy and fibrosis involving Smad3 signaling, suggesting that inhibition of gut microbes or generation of TMAO may become a potential target for the prevention and treatment of cardiac hypertrophy.</description><identifier>ISSN: 0023-6837</identifier><identifier>EISSN: 1530-0307</identifier><identifier>DOI: 10.1038/s41374-018-0091-y</identifier><identifier>PMID: 30068915</identifier><language>eng</language><publisher>New York: Elsevier Inc</publisher><subject>13/1 ; 14/34 ; 14/63 ; 631/80 ; 692/699/75/230 ; 82/1 ; 82/80 ; 82/81 ; Animals ; Antibiotics ; Aorta ; Atrial natriuretic peptide ; Cardiomegaly - etiology ; Cardiomegaly - metabolism ; Cardiomegaly - pathology ; Cardiomyocytes ; Cardiovascular diseases ; Cell size ; Cells, Cultured ; Choline ; Diet ; Disease Models, Animal ; Eutrophication ; Fibrosis ; Gastrointestinal Microbiome - physiology ; Health risks ; Heart ; Hypertrophy ; Inhibition ; Intestinal microflora ; Laboratory Medicine ; Male ; Medicine ; Medicine & Public Health ; Methylamines - antagonists & inhibitors ; Methylamines - metabolism ; Methylamines - toxicity ; Microorganisms ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; Myosin ; Nutrients ; Pathology ; Pharmacology ; Rats ; Rats, Sprague-Dawley ; Rodents ; Signal Transduction ; Smad3 protein ; Smad3 Protein - antagonists & inhibitors ; Smad3 Protein - metabolism ; Transforming Growth Factor beta1 - metabolism ; Trimethylamine</subject><ispartof>Laboratory investigation, 2019-03, Vol.99 (3), p.346-357</ispartof><rights>2018 United States & Canadian Academy of Pathology</rights><rights>United States & Canadian Academy of Pathology 2018</rights><rights>Copyright Nature Publishing Group Mar 2019</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c581t-fb1e67581e377528aef3154c9bc35a6ddf33329163c98bd9d23670a600f2893</citedby><cites>FETCH-LOGICAL-c581t-fb1e67581e377528aef3154c9bc35a6ddf33329163c98bd9d23670a600f2893</cites><orcidid>0000-0002-6962-1169</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,27931,27932</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30068915$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Zehua</creatorcontrib><creatorcontrib>Wu, Zhiye</creatorcontrib><creatorcontrib>Yan, Jianyun</creatorcontrib><creatorcontrib>Liu, Hailin</creatorcontrib><creatorcontrib>Liu, Qicai</creatorcontrib><creatorcontrib>Deng, Yi</creatorcontrib><creatorcontrib>Ou, Caiwen</creatorcontrib><creatorcontrib>Chen, Minsheng</creatorcontrib><title>Gut microbe-derived metabolite trimethylamine N-oxide induces cardiac hypertrophy and fibrosis</title><title>Laboratory investigation</title><addtitle>Lab Invest</addtitle><addtitle>Lab Invest</addtitle><description>Trimethylamine N-oxide (TMAO), a gut microbe-derived metabolite of dietary choline and other trimethylamine-containing nutrients, has been linked to increased cardiovascular disease risk. It is unknown whether TMAO plays a role in the development of cardiac hypertrophy. Transverse aortic constriction (TAC) was performed to induce cardiac hypertrophy in Sprague-Dawley (SD) rats. We observed that TMAO levels were significantly elevated in SD rats after 6 weeks of TAC, suggesting the potential role of TMAO in regulating cardiac hypertrophy. In cultured cardiomyocytes, TMAO treatment stimulated cardiac hypertrophy, as indicated by increased cell area of cardiomyocytes and expression of hypertrophic markers including atrial natriuretic peptide (ANP) and beta-myosin heavy chain (β-MHC). Additionally, TMAO treatment induced cardiac hypertrophy and cardiac fibrosis in SD rats. Reducing TMAO synthesis by antibiotics (Abs) attenuated TAC-induced cardiac hypertrophy and fibrosis. Furthermore, pharmacological inhibition of Smad3 by SIS3 significantly reduced the expression of ANP and β-MHC, and cardiomyocyte cell size in TMAO-treated group. These data for the first time demonstrate that gut microbe-derived metabolite TMAO induces cardiac hypertrophy and fibrosis involving Smad3 signaling, suggesting that inhibition of gut microbes or generation of TMAO may become a potential target for the prevention and treatment of cardiac hypertrophy.</description><subject>13/1</subject><subject>14/34</subject><subject>14/63</subject><subject>631/80</subject><subject>692/699/75/230</subject><subject>82/1</subject><subject>82/80</subject><subject>82/81</subject><subject>Animals</subject><subject>Antibiotics</subject><subject>Aorta</subject><subject>Atrial natriuretic peptide</subject><subject>Cardiomegaly - etiology</subject><subject>Cardiomegaly - metabolism</subject><subject>Cardiomegaly - pathology</subject><subject>Cardiomyocytes</subject><subject>Cardiovascular diseases</subject><subject>Cell size</subject><subject>Cells, Cultured</subject><subject>Choline</subject><subject>Diet</subject><subject>Disease Models, Animal</subject><subject>Eutrophication</subject><subject>Fibrosis</subject><subject>Gastrointestinal Microbiome - physiology</subject><subject>Health risks</subject><subject>Heart</subject><subject>Hypertrophy</subject><subject>Inhibition</subject><subject>Intestinal microflora</subject><subject>Laboratory Medicine</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Methylamines - antagonists & inhibitors</subject><subject>Methylamines - metabolism</subject><subject>Methylamines - toxicity</subject><subject>Microorganisms</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Myosin</subject><subject>Nutrients</subject><subject>Pathology</subject><subject>Pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Smad3 protein</subject><subject>Smad3 Protein - antagonists & inhibitors</subject><subject>Smad3 Protein - metabolism</subject><subject>Transforming Growth Factor beta1 - metabolism</subject><subject>Trimethylamine</subject><issn>0023-6837</issn><issn>1530-0307</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kE1P5SAUholx4r1-_AA3hsQ1eiiF0rgyxnFMzMxiZj2EwqmXm3vbK7TG_nsx9WPnCgjv856ch5BTDhcchL5MJRdVyYBrBlBzNu2RJZcCGAio9skSoBBMaVEtyGFKawBelkoekIUAULrmckn-340D3QYX-waZxxie0dMtDrbpN2FAOsSQX6tpY7ehQ_qb9S_BIw2dHx0m6mz0wTq6mnYYh9jvVhO1nadtaGKfQjomP1q7SXjyfh6Rvz9v_938Yg9_7u5vrh-Yk5oPrG04qipfUVSVLLTFVnBZurpxQlrlfSuEKGquhKt142tfCFWBVQBtoWtxRM7n1l3sn0ZMg1n3Y-zyQFNwrbgsZAU5xedUXjaliK3Z5eVsnAwH8-bTzD5N9mnefJopM2fvzWOzRf9JfAjMgWIOpPzVPWL8Gv1d69UMYVbyHDKUXMDOoQ8R3WB8H76hXwEuPJUC</recordid><startdate>20190301</startdate><enddate>20190301</enddate><creator>Li, Zehua</creator><creator>Wu, Zhiye</creator><creator>Yan, Jianyun</creator><creator>Liu, Hailin</creator><creator>Liu, Qicai</creator><creator>Deng, Yi</creator><creator>Ou, Caiwen</creator><creator>Chen, Minsheng</creator><general>Elsevier Inc</general><general>Nature Publishing Group US</general><general>Nature Publishing Group</general><scope>6I.</scope><scope>AAFTH</scope><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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><orcidid>https://orcid.org/0000-0002-6962-1169</orcidid></search><sort><creationdate>20190301</creationdate><title>Gut microbe-derived metabolite trimethylamine N-oxide induces cardiac hypertrophy and fibrosis</title><author>Li, Zehua ; Wu, Zhiye ; Yan, Jianyun ; Liu, Hailin ; Liu, Qicai ; Deng, Yi ; Ou, Caiwen ; Chen, Minsheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c581t-fb1e67581e377528aef3154c9bc35a6ddf33329163c98bd9d23670a600f2893</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>13/1</topic><topic>14/34</topic><topic>14/63</topic><topic>631/80</topic><topic>692/699/75/230</topic><topic>82/1</topic><topic>82/80</topic><topic>82/81</topic><topic>Animals</topic><topic>Antibiotics</topic><topic>Aorta</topic><topic>Atrial natriuretic peptide</topic><topic>Cardiomegaly - etiology</topic><topic>Cardiomegaly - metabolism</topic><topic>Cardiomegaly - pathology</topic><topic>Cardiomyocytes</topic><topic>Cardiovascular diseases</topic><topic>Cell size</topic><topic>Cells, Cultured</topic><topic>Choline</topic><topic>Diet</topic><topic>Disease Models, Animal</topic><topic>Eutrophication</topic><topic>Fibrosis</topic><topic>Gastrointestinal Microbiome - physiology</topic><topic>Health risks</topic><topic>Heart</topic><topic>Hypertrophy</topic><topic>Inhibition</topic><topic>Intestinal microflora</topic><topic>Laboratory Medicine</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Methylamines - antagonists & inhibitors</topic><topic>Methylamines - metabolism</topic><topic>Methylamines - toxicity</topic><topic>Microorganisms</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Myosin</topic><topic>Nutrients</topic><topic>Pathology</topic><topic>Pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rodents</topic><topic>Signal Transduction</topic><topic>Smad3 protein</topic><topic>Smad3 Protein - antagonists & inhibitors</topic><topic>Smad3 Protein - metabolism</topic><topic>Transforming Growth Factor beta1 - metabolism</topic><topic>Trimethylamine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Zehua</creatorcontrib><creatorcontrib>Wu, Zhiye</creatorcontrib><creatorcontrib>Yan, Jianyun</creatorcontrib><creatorcontrib>Liu, Hailin</creatorcontrib><creatorcontrib>Liu, Qicai</creatorcontrib><creatorcontrib>Deng, Yi</creatorcontrib><creatorcontrib>Ou, Caiwen</creatorcontrib><creatorcontrib>Chen, Minsheng</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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><jtitle>Laboratory investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Zehua</au><au>Wu, Zhiye</au><au>Yan, Jianyun</au><au>Liu, Hailin</au><au>Liu, Qicai</au><au>Deng, Yi</au><au>Ou, Caiwen</au><au>Chen, Minsheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gut microbe-derived metabolite trimethylamine N-oxide induces cardiac hypertrophy and fibrosis</atitle><jtitle>Laboratory investigation</jtitle><stitle>Lab Invest</stitle><addtitle>Lab Invest</addtitle><date>2019-03-01</date><risdate>2019</risdate><volume>99</volume><issue>3</issue><spage>346</spage><epage>357</epage><pages>346-357</pages><issn>0023-6837</issn><eissn>1530-0307</eissn><abstract>Trimethylamine N-oxide (TMAO), a gut microbe-derived metabolite of dietary choline and other trimethylamine-containing nutrients, has been linked to increased cardiovascular disease risk. It is unknown whether TMAO plays a role in the development of cardiac hypertrophy. Transverse aortic constriction (TAC) was performed to induce cardiac hypertrophy in Sprague-Dawley (SD) rats. We observed that TMAO levels were significantly elevated in SD rats after 6 weeks of TAC, suggesting the potential role of TMAO in regulating cardiac hypertrophy. In cultured cardiomyocytes, TMAO treatment stimulated cardiac hypertrophy, as indicated by increased cell area of cardiomyocytes and expression of hypertrophic markers including atrial natriuretic peptide (ANP) and beta-myosin heavy chain (β-MHC). Additionally, TMAO treatment induced cardiac hypertrophy and cardiac fibrosis in SD rats. Reducing TMAO synthesis by antibiotics (Abs) attenuated TAC-induced cardiac hypertrophy and fibrosis. Furthermore, pharmacological inhibition of Smad3 by SIS3 significantly reduced the expression of ANP and β-MHC, and cardiomyocyte cell size in TMAO-treated group. These data for the first time demonstrate that gut microbe-derived metabolite TMAO induces cardiac hypertrophy and fibrosis involving Smad3 signaling, suggesting that inhibition of gut microbes or generation of TMAO may become a potential target for the prevention and treatment of cardiac hypertrophy.</abstract><cop>New York</cop><pub>Elsevier Inc</pub><pmid>30068915</pmid><doi>10.1038/s41374-018-0091-y</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-6962-1169</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0023-6837 |
| ispartof | Laboratory investigation, 2019-03, Vol.99 (3), p.346-357 |
| issn | 0023-6837 1530-0307 |
| language | eng |
| recordid | cdi_proquest_journals_2186152570 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | 13/1 14/34 14/63 631/80 692/699/75/230 82/1 82/80 82/81 Animals Antibiotics Aorta Atrial natriuretic peptide Cardiomegaly - etiology Cardiomegaly - metabolism Cardiomegaly - pathology Cardiomyocytes Cardiovascular diseases Cell size Cells, Cultured Choline Diet Disease Models, Animal Eutrophication Fibrosis Gastrointestinal Microbiome - physiology Health risks Heart Hypertrophy Inhibition Intestinal microflora Laboratory Medicine Male Medicine Medicine & Public Health Methylamines - antagonists & inhibitors Methylamines - metabolism Methylamines - toxicity Microorganisms Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Myosin Nutrients Pathology Pharmacology Rats Rats, Sprague-Dawley Rodents Signal Transduction Smad3 protein Smad3 Protein - antagonists & inhibitors Smad3 Protein - metabolism Transforming Growth Factor beta1 - metabolism Trimethylamine |
| title | Gut microbe-derived metabolite trimethylamine N-oxide induces cardiac hypertrophy and fibrosis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-04T16%3A49%3A48IST&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=Gut%20microbe-derived%20metabolite%20trimethylamine%20N-oxide%20induces%20cardiac%20hypertrophy%20and%20fibrosis&rft.jtitle=Laboratory%20investigation&rft.au=Li,%20Zehua&rft.date=2019-03-01&rft.volume=99&rft.issue=3&rft.spage=346&rft.epage=357&rft.pages=346-357&rft.issn=0023-6837&rft.eissn=1530-0307&rft_id=info:doi/10.1038/s41374-018-0091-y&rft_dat=%3Cproquest_cross%3E2186152570%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=2186152570&rft_id=info:pmid/30068915&rft_els_id=S0023683722006778&rfr_iscdi=true |