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Characterization of left ventricular myocardial sodium-glucose cotransporter 1 expression in patients with end-stage heart failure
Whereas selective sodium-glucose cotransporter 2 (SGLT2) inhibitors consistently showed cardiovascular protective effects in large outcome trials independent of the presence of type 2 diabetes mellitus (T2DM), the cardiovascular effects of dual SGLT1/2 inhibitors remain to be elucidated. Despite its...
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Published in: | Cardiovascular diabetology 2020-09, Vol.19 (1), p.159-159, Article 159 |
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creator | Sayour, Alex Ali Oláh, Attila Ruppert, Mihály Barta, Bálint András Horváth, Eszter Mária Benke, Kálmán Pólos, Miklós Hartyánszky, István Merkely, Béla Radovits, Tamás |
description | Whereas selective sodium-glucose cotransporter 2 (SGLT2) inhibitors consistently showed cardiovascular protective effects in large outcome trials independent of the presence of type 2 diabetes mellitus (T2DM), the cardiovascular effects of dual SGLT1/2 inhibitors remain to be elucidated. Despite its clinical relevance, data are scarce regarding left ventricular (LV) SGLT1 expression in distinct heart failure (HF) pathologies. We aimed to characterize LV SGLT1 expression in human patients with end-stage HF, in context of the other two major glucose transporters: GLUT1 and GLUT4.
Control LV samples (Control, n = 9) were harvested from patients with preserved LV systolic function who went through mitral valve replacement. LV samples from HF patients undergoing heart transplantation (n = 71) were obtained according to the following etiological subgroups: hypertrophic cardiomyopathy (HCM, n = 7); idiopathic dilated cardiomyopathy (DCM, n = 12); ischemic heart disease without T2DM (IHD, n = 14), IHD with T2DM (IHD + T2DM, n = 11); and HF patients with cardiac resynchronization therapy (DCM:CRT, n = 9, IHD:CRT, n = 9 and IHD-T2DM:CRT, n = 9). We measured LV SGLT1, GLUT1 and GLUT4 gene expressions with qRT-PCR. The protein expression of SGLT1, and activating phosphorylation of AMP-activated protein kinase (AMPKα) and extracellular signal-regulated kinase 1/2 (ERK1/2) were quantified by western blotting. Immunohistochemical staining of SGLT1 was performed.
Compared with controls, LV SGLT1 mRNA and protein expressions were significantly and comparably upregulated in HF patients with DCM, IHD and IHD + T2DM (all P |
doi_str_mv | 10.1186/s12933-020-01141-1 |
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Control LV samples (Control, n = 9) were harvested from patients with preserved LV systolic function who went through mitral valve replacement. LV samples from HF patients undergoing heart transplantation (n = 71) were obtained according to the following etiological subgroups: hypertrophic cardiomyopathy (HCM, n = 7); idiopathic dilated cardiomyopathy (DCM, n = 12); ischemic heart disease without T2DM (IHD, n = 14), IHD with T2DM (IHD + T2DM, n = 11); and HF patients with cardiac resynchronization therapy (DCM:CRT, n = 9, IHD:CRT, n = 9 and IHD-T2DM:CRT, n = 9). We measured LV SGLT1, GLUT1 and GLUT4 gene expressions with qRT-PCR. The protein expression of SGLT1, and activating phosphorylation of AMP-activated protein kinase (AMPKα) and extracellular signal-regulated kinase 1/2 (ERK1/2) were quantified by western blotting. Immunohistochemical staining of SGLT1 was performed.
Compared with controls, LV SGLT1 mRNA and protein expressions were significantly and comparably upregulated in HF patients with DCM, IHD and IHD + T2DM (all P < 0.05), but not in HCM. LV SGLT1 mRNA and protein expressions positively correlated with LVEDD and negatively correlated with EF (all P < 0.01). Whereas AMPKα phosphorylation was positively associated with SGLT1 protein expression, ERK1/2 phosphorylation showed a negative correlation (both P < 0.01). Immunohistochemical staining revealed that SGLT1 expression was predominantly confined to cardiomyocytes, and not fibrotic tissue. Overall, CRT was associated with reduction of LV SGLT1 expression, especially in patients with DCM.
Myocardial LV SGLT1 is upregulated in patients with HF (except in those with HCM), correlates significantly with parameters of cardiac remodeling (LVEDD) and systolic function (EF), and is downregulated in DCM patients with CRT. The possible role of SGLT1 in LV remodeling needs to be elucidated.</description><identifier>ISSN: 1475-2840</identifier><identifier>EISSN: 1475-2840</identifier><identifier>DOI: 10.1186/s12933-020-01141-1</identifier><identifier>PMID: 32998746</identifier><language>eng</language><publisher>England: BioMed Central</publisher><subject>Adult ; Aged ; AMP ; AMP-activated protein kinase ; AMP-Activated Protein Kinases - analysis ; Atherosclerosis ; Biobanks ; Cardiac resynchronization therapy ; Cardiomyocytes ; Cardiomyopathy ; Cardiovascular disease ; Case-Control Studies ; Clinical trials ; Comorbidity ; Congestive heart failure ; Cooling ; Coronary artery disease ; Diabetes mellitus (non-insulin dependent) ; Dilated cardiomyopathy ; Dual SGLT1/2 inhibitors ; Ejection fraction ; Etiology ; Extracellular signal-regulated kinase ; Extracellular Signal-Regulated MAP Kinases - analysis ; Female ; Gene expression ; Gene Expression Regulation ; Glucose ; Glucose Transporter Type 1 - analysis ; Glucose Transporter Type 4 - analysis ; GLUT4 gene ; Heart failure ; Heart Failure - genetics ; Heart Failure - metabolism ; Heart Failure - physiopathology ; Heart Failure - therapy ; Heart transplantation ; Humans ; Hypertension ; Ischemia ; Laboratories ; Male ; Middle Aged ; Mitral valve ; mRNA ; Myocardium - chemistry ; Na+/glucose cotransporter ; Original Investigation ; Phosphorylation ; Polymerase chain reaction ; Rheumatic heart disease ; SGLT2 inhibitor ; Small intestine ; Sodium-glucose cotransporter 1 ; Sodium-Glucose Transporter 1 - analysis ; Sodium-Glucose Transporter 1 - genetics ; Sodium-Glucose Transporter 2 - analysis ; Ventricle ; Western blotting</subject><ispartof>Cardiovascular diabetology, 2020-09, Vol.19 (1), p.159-159, Article 159</ispartof><rights>2020. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c563t-5466f7edc9d107e02e3e13b17c5171ceeef6219ff8e509bec7292bc26cad7e63</citedby><cites>FETCH-LOGICAL-c563t-5466f7edc9d107e02e3e13b17c5171ceeef6219ff8e509bec7292bc26cad7e63</cites><orcidid>0000-0001-7728-4775</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7528261/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2451726951?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25732,27903,27904,36991,36992,44569,53770,53772</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32998746$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sayour, Alex Ali</creatorcontrib><creatorcontrib>Oláh, Attila</creatorcontrib><creatorcontrib>Ruppert, Mihály</creatorcontrib><creatorcontrib>Barta, Bálint András</creatorcontrib><creatorcontrib>Horváth, Eszter Mária</creatorcontrib><creatorcontrib>Benke, Kálmán</creatorcontrib><creatorcontrib>Pólos, Miklós</creatorcontrib><creatorcontrib>Hartyánszky, István</creatorcontrib><creatorcontrib>Merkely, Béla</creatorcontrib><creatorcontrib>Radovits, Tamás</creatorcontrib><title>Characterization of left ventricular myocardial sodium-glucose cotransporter 1 expression in patients with end-stage heart failure</title><title>Cardiovascular diabetology</title><addtitle>Cardiovasc Diabetol</addtitle><description>Whereas selective sodium-glucose cotransporter 2 (SGLT2) inhibitors consistently showed cardiovascular protective effects in large outcome trials independent of the presence of type 2 diabetes mellitus (T2DM), the cardiovascular effects of dual SGLT1/2 inhibitors remain to be elucidated. Despite its clinical relevance, data are scarce regarding left ventricular (LV) SGLT1 expression in distinct heart failure (HF) pathologies. We aimed to characterize LV SGLT1 expression in human patients with end-stage HF, in context of the other two major glucose transporters: GLUT1 and GLUT4.
Control LV samples (Control, n = 9) were harvested from patients with preserved LV systolic function who went through mitral valve replacement. LV samples from HF patients undergoing heart transplantation (n = 71) were obtained according to the following etiological subgroups: hypertrophic cardiomyopathy (HCM, n = 7); idiopathic dilated cardiomyopathy (DCM, n = 12); ischemic heart disease without T2DM (IHD, n = 14), IHD with T2DM (IHD + T2DM, n = 11); and HF patients with cardiac resynchronization therapy (DCM:CRT, n = 9, IHD:CRT, n = 9 and IHD-T2DM:CRT, n = 9). We measured LV SGLT1, GLUT1 and GLUT4 gene expressions with qRT-PCR. The protein expression of SGLT1, and activating phosphorylation of AMP-activated protein kinase (AMPKα) and extracellular signal-regulated kinase 1/2 (ERK1/2) were quantified by western blotting. Immunohistochemical staining of SGLT1 was performed.
Compared with controls, LV SGLT1 mRNA and protein expressions were significantly and comparably upregulated in HF patients with DCM, IHD and IHD + T2DM (all P < 0.05), but not in HCM. LV SGLT1 mRNA and protein expressions positively correlated with LVEDD and negatively correlated with EF (all P < 0.01). Whereas AMPKα phosphorylation was positively associated with SGLT1 protein expression, ERK1/2 phosphorylation showed a negative correlation (both P < 0.01). Immunohistochemical staining revealed that SGLT1 expression was predominantly confined to cardiomyocytes, and not fibrotic tissue. Overall, CRT was associated with reduction of LV SGLT1 expression, especially in patients with DCM.
Myocardial LV SGLT1 is upregulated in patients with HF (except in those with HCM), correlates significantly with parameters of cardiac remodeling (LVEDD) and systolic function (EF), and is downregulated in DCM patients with CRT. The possible role of SGLT1 in LV remodeling needs to be elucidated.</description><subject>Adult</subject><subject>Aged</subject><subject>AMP</subject><subject>AMP-activated protein kinase</subject><subject>AMP-Activated Protein Kinases - analysis</subject><subject>Atherosclerosis</subject><subject>Biobanks</subject><subject>Cardiac resynchronization therapy</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathy</subject><subject>Cardiovascular disease</subject><subject>Case-Control Studies</subject><subject>Clinical trials</subject><subject>Comorbidity</subject><subject>Congestive heart failure</subject><subject>Cooling</subject><subject>Coronary artery disease</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Dilated cardiomyopathy</subject><subject>Dual SGLT1/2 inhibitors</subject><subject>Ejection fraction</subject><subject>Etiology</subject><subject>Extracellular signal-regulated kinase</subject><subject>Extracellular Signal-Regulated MAP Kinases - analysis</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Glucose</subject><subject>Glucose Transporter Type 1 - analysis</subject><subject>Glucose Transporter Type 4 - analysis</subject><subject>GLUT4 gene</subject><subject>Heart failure</subject><subject>Heart Failure - genetics</subject><subject>Heart Failure - metabolism</subject><subject>Heart Failure - physiopathology</subject><subject>Heart Failure - therapy</subject><subject>Heart transplantation</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Ischemia</subject><subject>Laboratories</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Mitral valve</subject><subject>mRNA</subject><subject>Myocardium - chemistry</subject><subject>Na+/glucose cotransporter</subject><subject>Original Investigation</subject><subject>Phosphorylation</subject><subject>Polymerase chain reaction</subject><subject>Rheumatic heart disease</subject><subject>SGLT2 inhibitor</subject><subject>Small intestine</subject><subject>Sodium-glucose cotransporter 1</subject><subject>Sodium-Glucose Transporter 1 - analysis</subject><subject>Sodium-Glucose Transporter 1 - genetics</subject><subject>Sodium-Glucose Transporter 2 - analysis</subject><subject>Ventricle</subject><subject>Western blotting</subject><issn>1475-2840</issn><issn>1475-2840</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdkktv1DAUhSMEoqXwB1ggS2y6Cfg6jh8bJDTiUakSm-4tx7mZ8SiJB9splCW_vE6nVC0rW_a5n849OlX1FugHACU-JmC6aWrKaE0BONTwrDoFLtuaKU6fP7qfVK9S2lMKUgl4WZ00TGsluTit_m52NlqXMfo_NvswkzCQEYdMrnHO0btltJFMN8HZ2Hs7khR6v0z1dlxcSEhcyNHO6RBiQRAg-PsQMaUV5GdyKMiCSeSXzzuCc1-nbLdIdmhjJoP14xLxdfVisGPCN_fnWXX19cvV5nt9-ePbxebzZe1a0eS65UIMEnune6ASKcMGoelAuhYkOEQcBAM9DApbqjt0kmnWOSac7SWK5qy6OGL7YPfmEP1k440J1pu7hxC3ppjybkSjHXZtw3VJTnGuUHPdUSspB4Vi6GRhfTqyDks3FUtrVHZ8An36M_ud2YZrI1ummIACOL8HxPBzwZTN5JPDcbQzhiUZxrlUnDFFi_T9f9J9WOJckiqqsjoTul2B7KhyMaQUcXgwA9SsbTHHtpjSFnPXFrMOvXu8xsPIv3o0t0_vvl0</recordid><startdate>20200930</startdate><enddate>20200930</enddate><creator>Sayour, Alex Ali</creator><creator>Oláh, Attila</creator><creator>Ruppert, Mihály</creator><creator>Barta, Bálint András</creator><creator>Horváth, Eszter Mária</creator><creator>Benke, Kálmán</creator><creator>Pólos, Miklós</creator><creator>Hartyánszky, István</creator><creator>Merkely, Béla</creator><creator>Radovits, Tamás</creator><general>BioMed Central</general><general>BMC</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>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-7728-4775</orcidid></search><sort><creationdate>20200930</creationdate><title>Characterization of left ventricular myocardial sodium-glucose cotransporter 1 expression in patients with end-stage heart failure</title><author>Sayour, Alex Ali ; Oláh, Attila ; Ruppert, Mihály ; Barta, Bálint András ; Horváth, Eszter Mária ; Benke, Kálmán ; Pólos, Miklós ; Hartyánszky, István ; Merkely, Béla ; Radovits, Tamás</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c563t-5466f7edc9d107e02e3e13b17c5171ceeef6219ff8e509bec7292bc26cad7e63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Adult</topic><topic>Aged</topic><topic>AMP</topic><topic>AMP-activated protein kinase</topic><topic>AMP-Activated Protein Kinases - 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genetics</topic><topic>Heart Failure - metabolism</topic><topic>Heart Failure - physiopathology</topic><topic>Heart Failure - therapy</topic><topic>Heart transplantation</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Ischemia</topic><topic>Laboratories</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Mitral valve</topic><topic>mRNA</topic><topic>Myocardium - chemistry</topic><topic>Na+/glucose cotransporter</topic><topic>Original Investigation</topic><topic>Phosphorylation</topic><topic>Polymerase chain reaction</topic><topic>Rheumatic heart disease</topic><topic>SGLT2 inhibitor</topic><topic>Small intestine</topic><topic>Sodium-glucose cotransporter 1</topic><topic>Sodium-Glucose Transporter 1 - analysis</topic><topic>Sodium-Glucose Transporter 1 - genetics</topic><topic>Sodium-Glucose Transporter 2 - analysis</topic><topic>Ventricle</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sayour, Alex Ali</creatorcontrib><creatorcontrib>Oláh, Attila</creatorcontrib><creatorcontrib>Ruppert, Mihály</creatorcontrib><creatorcontrib>Barta, Bálint András</creatorcontrib><creatorcontrib>Horváth, Eszter Mária</creatorcontrib><creatorcontrib>Benke, Kálmán</creatorcontrib><creatorcontrib>Pólos, Miklós</creatorcontrib><creatorcontrib>Hartyánszky, István</creatorcontrib><creatorcontrib>Merkely, Béla</creatorcontrib><creatorcontrib>Radovits, Tamás</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>Immunology Abstracts</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content (ProQuest)</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cardiovascular diabetology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sayour, Alex Ali</au><au>Oláh, Attila</au><au>Ruppert, Mihály</au><au>Barta, Bálint András</au><au>Horváth, Eszter Mária</au><au>Benke, Kálmán</au><au>Pólos, Miklós</au><au>Hartyánszky, István</au><au>Merkely, Béla</au><au>Radovits, Tamás</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Characterization of left ventricular myocardial sodium-glucose cotransporter 1 expression in patients with end-stage heart failure</atitle><jtitle>Cardiovascular diabetology</jtitle><addtitle>Cardiovasc Diabetol</addtitle><date>2020-09-30</date><risdate>2020</risdate><volume>19</volume><issue>1</issue><spage>159</spage><epage>159</epage><pages>159-159</pages><artnum>159</artnum><issn>1475-2840</issn><eissn>1475-2840</eissn><abstract>Whereas selective sodium-glucose cotransporter 2 (SGLT2) inhibitors consistently showed cardiovascular protective effects in large outcome trials independent of the presence of type 2 diabetes mellitus (T2DM), the cardiovascular effects of dual SGLT1/2 inhibitors remain to be elucidated. Despite its clinical relevance, data are scarce regarding left ventricular (LV) SGLT1 expression in distinct heart failure (HF) pathologies. We aimed to characterize LV SGLT1 expression in human patients with end-stage HF, in context of the other two major glucose transporters: GLUT1 and GLUT4.
Control LV samples (Control, n = 9) were harvested from patients with preserved LV systolic function who went through mitral valve replacement. LV samples from HF patients undergoing heart transplantation (n = 71) were obtained according to the following etiological subgroups: hypertrophic cardiomyopathy (HCM, n = 7); idiopathic dilated cardiomyopathy (DCM, n = 12); ischemic heart disease without T2DM (IHD, n = 14), IHD with T2DM (IHD + T2DM, n = 11); and HF patients with cardiac resynchronization therapy (DCM:CRT, n = 9, IHD:CRT, n = 9 and IHD-T2DM:CRT, n = 9). We measured LV SGLT1, GLUT1 and GLUT4 gene expressions with qRT-PCR. The protein expression of SGLT1, and activating phosphorylation of AMP-activated protein kinase (AMPKα) and extracellular signal-regulated kinase 1/2 (ERK1/2) were quantified by western blotting. Immunohistochemical staining of SGLT1 was performed.
Compared with controls, LV SGLT1 mRNA and protein expressions were significantly and comparably upregulated in HF patients with DCM, IHD and IHD + T2DM (all P < 0.05), but not in HCM. LV SGLT1 mRNA and protein expressions positively correlated with LVEDD and negatively correlated with EF (all P < 0.01). Whereas AMPKα phosphorylation was positively associated with SGLT1 protein expression, ERK1/2 phosphorylation showed a negative correlation (both P < 0.01). Immunohistochemical staining revealed that SGLT1 expression was predominantly confined to cardiomyocytes, and not fibrotic tissue. Overall, CRT was associated with reduction of LV SGLT1 expression, especially in patients with DCM.
Myocardial LV SGLT1 is upregulated in patients with HF (except in those with HCM), correlates significantly with parameters of cardiac remodeling (LVEDD) and systolic function (EF), and is downregulated in DCM patients with CRT. The possible role of SGLT1 in LV remodeling needs to be elucidated.</abstract><cop>England</cop><pub>BioMed Central</pub><pmid>32998746</pmid><doi>10.1186/s12933-020-01141-1</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-7728-4775</orcidid><oa>free_for_read</oa></addata></record> |
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recordid | cdi_doaj_primary_oai_doaj_org_article_9ceb53498408448e949b0a70418e6fb7 |
source | Publicly Available Content (ProQuest); PubMed Central |
subjects | Adult Aged AMP AMP-activated protein kinase AMP-Activated Protein Kinases - analysis Atherosclerosis Biobanks Cardiac resynchronization therapy Cardiomyocytes Cardiomyopathy Cardiovascular disease Case-Control Studies Clinical trials Comorbidity Congestive heart failure Cooling Coronary artery disease Diabetes mellitus (non-insulin dependent) Dilated cardiomyopathy Dual SGLT1/2 inhibitors Ejection fraction Etiology Extracellular signal-regulated kinase Extracellular Signal-Regulated MAP Kinases - analysis Female Gene expression Gene Expression Regulation Glucose Glucose Transporter Type 1 - analysis Glucose Transporter Type 4 - analysis GLUT4 gene Heart failure Heart Failure - genetics Heart Failure - metabolism Heart Failure - physiopathology Heart Failure - therapy Heart transplantation Humans Hypertension Ischemia Laboratories Male Middle Aged Mitral valve mRNA Myocardium - chemistry Na+/glucose cotransporter Original Investigation Phosphorylation Polymerase chain reaction Rheumatic heart disease SGLT2 inhibitor Small intestine Sodium-glucose cotransporter 1 Sodium-Glucose Transporter 1 - analysis Sodium-Glucose Transporter 1 - genetics Sodium-Glucose Transporter 2 - analysis Ventricle Western blotting |
title | Characterization of left ventricular myocardial sodium-glucose cotransporter 1 expression in patients with end-stage heart failure |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-22T23%3A07%3A46IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_doaj_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Characterization%20of%20left%20ventricular%20myocardial%20sodium-glucose%20cotransporter%201%20expression%20in%20patients%20with%20end-stage%20heart%20failure&rft.jtitle=Cardiovascular%20diabetology&rft.au=Sayour,%20Alex%20Ali&rft.date=2020-09-30&rft.volume=19&rft.issue=1&rft.spage=159&rft.epage=159&rft.pages=159-159&rft.artnum=159&rft.issn=1475-2840&rft.eissn=1475-2840&rft_id=info:doi/10.1186/s12933-020-01141-1&rft_dat=%3Cproquest_doaj_%3E2451726951%3C/proquest_doaj_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c563t-5466f7edc9d107e02e3e13b17c5171ceeef6219ff8e509bec7292bc26cad7e63%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2451726951&rft_id=info:pmid/32998746&rfr_iscdi=true |