β-receptor antagonist treatment prevents activation of cell death signaling in the diabetic heart independent of its metabolic actions
We have previously shown that metoprolol improves function in the diabetic heart, associated with inhibition of fatty acid oxidation and a shift towards protein kinase B signaling. The aim of this study was to determine the relative importance of these metabolic and signaling effects to the preventi...
Gespeichert in:
| Veröffentlicht in: | European journal of pharmacology 2011-04, Vol.657 (1), p.117-125 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 125 |
|---|---|
| container_issue | 1 |
| container_start_page | 117 |
| container_title | European journal of pharmacology |
| container_volume | 657 |
| creator | Sharma, Vijay Sharma, Arpeeta Saran, Varun Bernatchez, Pascal N. Allard, Michael F. McNeill, John H. |
| description | We have previously shown that metoprolol improves function in the diabetic heart, associated with inhibition of fatty acid oxidation and a shift towards protein kinase B signaling. The aim of this study was to determine the relative importance of these metabolic and signaling effects to the prevention of cellular damage. Diabetes was induced in male Wistar rats by a single IV injection of 60
mg/kg streptozotocin, and treated groups received 15
mg/kg/day metoprolol delivered subcutaneously by osmotic pumps. Echocardiography was performed 6
weeks after streptozotocin injection, and the hearts immediately excised for histological and biochemical measurements of lipotoxicity, apoptosis, signaling and caveolin/caspase interactions. Metoprolol improved stroke volume and cardiac output, associated with attenuation of TUNEL staining and a more modest attenuation of caspase-3; however, the positive TUNEL staining was not associated with an increase in apoptosis or cell regeneration markers. Metoprolol inhibited CPT-1 without affecting CD36 translocation, associated with increased accumulation of triglycerides and long chain acyl CoA in the cytoplasm, and no effect on oxidative stress. Metoprolol induced a shift from protein kinase A to protein kinase B-mediated signaling, associated with a shift in the phosphorylation patterns of BCl-2 and Bad which favored BCl-2 action. Metoprolol also increased the interaction of activated caspase-3 with caveolins 1 and 3 outside caveolae. The actions of metoprolol on fatty acid oxidation do not prevent lipotoxicity; its beneficial effect is more likely to be due to pro-survival signaling and sequestration of activated caspase-3 by caveolins. |
| doi_str_mv | 10.1016/j.ejphar.2011.01.044 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1562670720</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0014299911001026</els_id><sourcerecordid>1562670720</sourcerecordid><originalsourceid>FETCH-LOGICAL-c448t-b901d5efad2596d4f429ada2b86a13364fb1aef1eef97e89b463d7b8f0cfde543</originalsourceid><addsrcrecordid>eNp9kd2KFDEQhRtR3HH1DURzI3jTY5JO_-RGWBb_YMEL3etQnVRmMvQkbZIZ8Al8Hx_EZzJNj3onFCkIX52T1Kmq54xuGWXdm8MWD_Me4pZTxra0lBAPqg0belnTnvGH1YZSJmoupbyqnqR0oJS2krePqyvOuOxo12yqH79-1hE1zjlEAj7DLniXMskRIR_RZzJHPJeeCOjszpBd8CRYonGaiCnQniS38zA5vyPOk7xHYhyMmJ0me4SYy63BGctR1MqkK1pHzDCGqSCLavDpafXIwpTw2aVfV_fv3329_Vjfff7w6fbmrtZCDLkeJWWmRQuGt7IzwgouwQAfhw5Y03TCjgzQMkQrexzkKLrG9ONgqbYGW9FcV69X3TmGbydMWR1dWv4CHsMpKdZ2vOtpz2lBxYrqGFKKaNUc3RHid8WoWiJQB7VGoJYIFC0lFocXF4fTeETzd-jPzgvw6gJA0jDZCF679I9rZNe2vC3cy5WzEBTsYmHuvxSntuQoKB0W4u1KYNnY2WFUSTv0Go0rmWZlgvv_W38DRvW0Aw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1562670720</pqid></control><display><type>article</type><title>β-receptor antagonist treatment prevents activation of cell death signaling in the diabetic heart independent of its metabolic actions</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals Complete</source><creator>Sharma, Vijay ; Sharma, Arpeeta ; Saran, Varun ; Bernatchez, Pascal N. ; Allard, Michael F. ; McNeill, John H.</creator><creatorcontrib>Sharma, Vijay ; Sharma, Arpeeta ; Saran, Varun ; Bernatchez, Pascal N. ; Allard, Michael F. ; McNeill, John H.</creatorcontrib><description>We have previously shown that metoprolol improves function in the diabetic heart, associated with inhibition of fatty acid oxidation and a shift towards protein kinase B signaling. The aim of this study was to determine the relative importance of these metabolic and signaling effects to the prevention of cellular damage. Diabetes was induced in male Wistar rats by a single IV injection of 60
mg/kg streptozotocin, and treated groups received 15
mg/kg/day metoprolol delivered subcutaneously by osmotic pumps. Echocardiography was performed 6
weeks after streptozotocin injection, and the hearts immediately excised for histological and biochemical measurements of lipotoxicity, apoptosis, signaling and caveolin/caspase interactions. Metoprolol improved stroke volume and cardiac output, associated with attenuation of TUNEL staining and a more modest attenuation of caspase-3; however, the positive TUNEL staining was not associated with an increase in apoptosis or cell regeneration markers. Metoprolol inhibited CPT-1 without affecting CD36 translocation, associated with increased accumulation of triglycerides and long chain acyl CoA in the cytoplasm, and no effect on oxidative stress. Metoprolol induced a shift from protein kinase A to protein kinase B-mediated signaling, associated with a shift in the phosphorylation patterns of BCl-2 and Bad which favored BCl-2 action. Metoprolol also increased the interaction of activated caspase-3 with caveolins 1 and 3 outside caveolae. The actions of metoprolol on fatty acid oxidation do not prevent lipotoxicity; its beneficial effect is more likely to be due to pro-survival signaling and sequestration of activated caspase-3 by caveolins.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/j.ejphar.2011.01.044</identifier><identifier>PMID: 21296063</identifier><identifier>CODEN: EJPHAZ</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>acyl coenzyme A ; Adrenergic beta-Antagonists - pharmacology ; Animals ; antagonists ; apoptosis ; bcl-Associated Death Protein - metabolism ; Biological and medical sciences ; cAMP-dependent protein kinase ; Cardiac metabolism ; cardiac output ; Cardiology. Vascular system ; Caspase 3 - metabolism ; caspase-3 ; Caveolins - metabolism ; Cell death ; Cell Death - drug effects ; Cyclic AMP-Dependent Protein Kinases - metabolism ; cytoplasm ; Diabetes ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Experimental - pathology ; Diabetes. Impaired glucose tolerance ; echocardiography ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; fatty acids ; Fatty Acids - metabolism ; Fatty Acids - toxicity ; Fibrosis - metabolism ; Heart ; Heart - drug effects ; Heart failure ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; intravenous injection ; long chain triacylglycerols ; Male ; Medical sciences ; Metoprolol - pharmacology ; Myocardium - metabolism ; Myocardium - pathology ; oxidation ; Oxidation-Reduction - drug effects ; Oxidative stress ; Oxidative Stress - drug effects ; pharmacology ; Pharmacology. Drug treatments ; phosphorylation ; Phosphorylation - drug effects ; Proto-Oncogene Proteins c-akt - metabolism ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; pumps ; Rats ; Rats, Wistar ; Receptors, Adrenergic, beta - metabolism ; Signal Transduction - drug effects ; streptozotocin ; β-receptor antagonist</subject><ispartof>European journal of pharmacology, 2011-04, Vol.657 (1), p.117-125</ispartof><rights>2011 Elsevier B.V.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c448t-b901d5efad2596d4f429ada2b86a13364fb1aef1eef97e89b463d7b8f0cfde543</citedby><cites>FETCH-LOGICAL-c448t-b901d5efad2596d4f429ada2b86a13364fb1aef1eef97e89b463d7b8f0cfde543</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ejphar.2011.01.044$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23965525$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21296063$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sharma, Vijay</creatorcontrib><creatorcontrib>Sharma, Arpeeta</creatorcontrib><creatorcontrib>Saran, Varun</creatorcontrib><creatorcontrib>Bernatchez, Pascal N.</creatorcontrib><creatorcontrib>Allard, Michael F.</creatorcontrib><creatorcontrib>McNeill, John H.</creatorcontrib><title>β-receptor antagonist treatment prevents activation of cell death signaling in the diabetic heart independent of its metabolic actions</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>We have previously shown that metoprolol improves function in the diabetic heart, associated with inhibition of fatty acid oxidation and a shift towards protein kinase B signaling. The aim of this study was to determine the relative importance of these metabolic and signaling effects to the prevention of cellular damage. Diabetes was induced in male Wistar rats by a single IV injection of 60
mg/kg streptozotocin, and treated groups received 15
mg/kg/day metoprolol delivered subcutaneously by osmotic pumps. Echocardiography was performed 6
weeks after streptozotocin injection, and the hearts immediately excised for histological and biochemical measurements of lipotoxicity, apoptosis, signaling and caveolin/caspase interactions. Metoprolol improved stroke volume and cardiac output, associated with attenuation of TUNEL staining and a more modest attenuation of caspase-3; however, the positive TUNEL staining was not associated with an increase in apoptosis or cell regeneration markers. Metoprolol inhibited CPT-1 without affecting CD36 translocation, associated with increased accumulation of triglycerides and long chain acyl CoA in the cytoplasm, and no effect on oxidative stress. Metoprolol induced a shift from protein kinase A to protein kinase B-mediated signaling, associated with a shift in the phosphorylation patterns of BCl-2 and Bad which favored BCl-2 action. Metoprolol also increased the interaction of activated caspase-3 with caveolins 1 and 3 outside caveolae. The actions of metoprolol on fatty acid oxidation do not prevent lipotoxicity; its beneficial effect is more likely to be due to pro-survival signaling and sequestration of activated caspase-3 by caveolins.</description><subject>acyl coenzyme A</subject><subject>Adrenergic beta-Antagonists - pharmacology</subject><subject>Animals</subject><subject>antagonists</subject><subject>apoptosis</subject><subject>bcl-Associated Death Protein - metabolism</subject><subject>Biological and medical sciences</subject><subject>cAMP-dependent protein kinase</subject><subject>Cardiac metabolism</subject><subject>cardiac output</subject><subject>Cardiology. Vascular system</subject><subject>Caspase 3 - metabolism</subject><subject>caspase-3</subject><subject>Caveolins - metabolism</subject><subject>Cell death</subject><subject>Cell Death - drug effects</subject><subject>Cyclic AMP-Dependent Protein Kinases - metabolism</subject><subject>cytoplasm</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Experimental - pathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>echocardiography</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>fatty acids</subject><subject>Fatty Acids - metabolism</subject><subject>Fatty Acids - toxicity</subject><subject>Fibrosis - metabolism</subject><subject>Heart</subject><subject>Heart - drug effects</subject><subject>Heart failure</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>intravenous injection</subject><subject>long chain triacylglycerols</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metoprolol - pharmacology</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - pathology</subject><subject>oxidation</subject><subject>Oxidation-Reduction - drug effects</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>pumps</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Adrenergic, beta - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>streptozotocin</subject><subject>β-receptor antagonist</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kd2KFDEQhRtR3HH1DURzI3jTY5JO_-RGWBb_YMEL3etQnVRmMvQkbZIZ8Al8Hx_EZzJNj3onFCkIX52T1Kmq54xuGWXdm8MWD_Me4pZTxra0lBAPqg0belnTnvGH1YZSJmoupbyqnqR0oJS2krePqyvOuOxo12yqH79-1hE1zjlEAj7DLniXMskRIR_RZzJHPJeeCOjszpBd8CRYonGaiCnQniS38zA5vyPOk7xHYhyMmJ0me4SYy63BGctR1MqkK1pHzDCGqSCLavDpafXIwpTw2aVfV_fv3329_Vjfff7w6fbmrtZCDLkeJWWmRQuGt7IzwgouwQAfhw5Y03TCjgzQMkQrexzkKLrG9ONgqbYGW9FcV69X3TmGbydMWR1dWv4CHsMpKdZ2vOtpz2lBxYrqGFKKaNUc3RHid8WoWiJQB7VGoJYIFC0lFocXF4fTeETzd-jPzgvw6gJA0jDZCF679I9rZNe2vC3cy5WzEBTsYmHuvxSntuQoKB0W4u1KYNnY2WFUSTv0Go0rmWZlgvv_W38DRvW0Aw</recordid><startdate>20110425</startdate><enddate>20110425</enddate><creator>Sharma, Vijay</creator><creator>Sharma, Arpeeta</creator><creator>Saran, Varun</creator><creator>Bernatchez, Pascal N.</creator><creator>Allard, Michael F.</creator><creator>McNeill, John H.</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>FBQ</scope><scope>IQODW</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>7U7</scope><scope>C1K</scope></search><sort><creationdate>20110425</creationdate><title>β-receptor antagonist treatment prevents activation of cell death signaling in the diabetic heart independent of its metabolic actions</title><author>Sharma, Vijay ; Sharma, Arpeeta ; Saran, Varun ; Bernatchez, Pascal N. ; Allard, Michael F. ; McNeill, John H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c448t-b901d5efad2596d4f429ada2b86a13364fb1aef1eef97e89b463d7b8f0cfde543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>acyl coenzyme A</topic><topic>Adrenergic beta-Antagonists - pharmacology</topic><topic>Animals</topic><topic>antagonists</topic><topic>apoptosis</topic><topic>bcl-Associated Death Protein - metabolism</topic><topic>Biological and medical sciences</topic><topic>cAMP-dependent protein kinase</topic><topic>Cardiac metabolism</topic><topic>cardiac output</topic><topic>Cardiology. Vascular system</topic><topic>Caspase 3 - metabolism</topic><topic>caspase-3</topic><topic>Caveolins - metabolism</topic><topic>Cell death</topic><topic>Cell Death - drug effects</topic><topic>Cyclic AMP-Dependent Protein Kinases - metabolism</topic><topic>cytoplasm</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes Mellitus, Experimental - pathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>echocardiography</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>fatty acids</topic><topic>Fatty Acids - metabolism</topic><topic>Fatty Acids - toxicity</topic><topic>Fibrosis - metabolism</topic><topic>Heart</topic><topic>Heart - drug effects</topic><topic>Heart failure</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>intravenous injection</topic><topic>long chain triacylglycerols</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metoprolol - pharmacology</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - pathology</topic><topic>oxidation</topic><topic>Oxidation-Reduction - drug effects</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>pharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>phosphorylation</topic><topic>Phosphorylation - drug effects</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>pumps</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, Adrenergic, beta - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>streptozotocin</topic><topic>β-receptor antagonist</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sharma, Vijay</creatorcontrib><creatorcontrib>Sharma, Arpeeta</creatorcontrib><creatorcontrib>Saran, Varun</creatorcontrib><creatorcontrib>Bernatchez, Pascal N.</creatorcontrib><creatorcontrib>Allard, Michael F.</creatorcontrib><creatorcontrib>McNeill, John H.</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sharma, Vijay</au><au>Sharma, Arpeeta</au><au>Saran, Varun</au><au>Bernatchez, Pascal N.</au><au>Allard, Michael F.</au><au>McNeill, John H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>β-receptor antagonist treatment prevents activation of cell death signaling in the diabetic heart independent of its metabolic actions</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2011-04-25</date><risdate>2011</risdate><volume>657</volume><issue>1</issue><spage>117</spage><epage>125</epage><pages>117-125</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>We have previously shown that metoprolol improves function in the diabetic heart, associated with inhibition of fatty acid oxidation and a shift towards protein kinase B signaling. The aim of this study was to determine the relative importance of these metabolic and signaling effects to the prevention of cellular damage. Diabetes was induced in male Wistar rats by a single IV injection of 60
mg/kg streptozotocin, and treated groups received 15
mg/kg/day metoprolol delivered subcutaneously by osmotic pumps. Echocardiography was performed 6
weeks after streptozotocin injection, and the hearts immediately excised for histological and biochemical measurements of lipotoxicity, apoptosis, signaling and caveolin/caspase interactions. Metoprolol improved stroke volume and cardiac output, associated with attenuation of TUNEL staining and a more modest attenuation of caspase-3; however, the positive TUNEL staining was not associated with an increase in apoptosis or cell regeneration markers. Metoprolol inhibited CPT-1 without affecting CD36 translocation, associated with increased accumulation of triglycerides and long chain acyl CoA in the cytoplasm, and no effect on oxidative stress. Metoprolol induced a shift from protein kinase A to protein kinase B-mediated signaling, associated with a shift in the phosphorylation patterns of BCl-2 and Bad which favored BCl-2 action. Metoprolol also increased the interaction of activated caspase-3 with caveolins 1 and 3 outside caveolae. The actions of metoprolol on fatty acid oxidation do not prevent lipotoxicity; its beneficial effect is more likely to be due to pro-survival signaling and sequestration of activated caspase-3 by caveolins.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>21296063</pmid><doi>10.1016/j.ejphar.2011.01.044</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0014-2999 |
| ispartof | European journal of pharmacology, 2011-04, Vol.657 (1), p.117-125 |
| issn | 0014-2999 1879-0712 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1562670720 |
| source | MEDLINE; Elsevier ScienceDirect Journals Complete |
| subjects | acyl coenzyme A Adrenergic beta-Antagonists - pharmacology Animals antagonists apoptosis bcl-Associated Death Protein - metabolism Biological and medical sciences cAMP-dependent protein kinase Cardiac metabolism cardiac output Cardiology. Vascular system Caspase 3 - metabolism caspase-3 Caveolins - metabolism Cell death Cell Death - drug effects Cyclic AMP-Dependent Protein Kinases - metabolism cytoplasm Diabetes Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - pathology Diabetes. Impaired glucose tolerance echocardiography Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance fatty acids Fatty Acids - metabolism Fatty Acids - toxicity Fibrosis - metabolism Heart Heart - drug effects Heart failure Heart failure, cardiogenic pulmonary edema, cardiac enlargement intravenous injection long chain triacylglycerols Male Medical sciences Metoprolol - pharmacology Myocardium - metabolism Myocardium - pathology oxidation Oxidation-Reduction - drug effects Oxidative stress Oxidative Stress - drug effects pharmacology Pharmacology. Drug treatments phosphorylation Phosphorylation - drug effects Proto-Oncogene Proteins c-akt - metabolism Proto-Oncogene Proteins c-bcl-2 - metabolism pumps Rats Rats, Wistar Receptors, Adrenergic, beta - metabolism Signal Transduction - drug effects streptozotocin β-receptor antagonist |
| title | β-receptor antagonist treatment prevents activation of cell death signaling in the diabetic heart independent of its metabolic actions |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-01T19%3A50%3A16IST&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=%CE%B2-receptor%20antagonist%20treatment%20prevents%20activation%20of%20cell%20death%20signaling%20in%20the%20diabetic%20heart%20independent%20of%20its%20metabolic%20actions&rft.jtitle=European%20journal%20of%20pharmacology&rft.au=Sharma,%20Vijay&rft.date=2011-04-25&rft.volume=657&rft.issue=1&rft.spage=117&rft.epage=125&rft.pages=117-125&rft.issn=0014-2999&rft.eissn=1879-0712&rft.coden=EJPHAZ&rft_id=info:doi/10.1016/j.ejphar.2011.01.044&rft_dat=%3Cproquest_cross%3E1562670720%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=1562670720&rft_id=info:pmid/21296063&rft_els_id=S0014299911001026&rfr_iscdi=true |