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Chronic Metformin Associated Cardioprotection Against Infarction: Not Just a Glucose Lowering Phenomenon
Purpose Clinical and experimental investigations demonstrated that metformin, a widely used anti-diabetic drug, exhibits cardioprotective properties against myocardial infarction. Interestingly, metformin was previously shown to increase the expression of PGC-1α a key controller of energy metabolism...
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| Published in: | Cardiovascular drugs and therapy 2013-02, Vol.27 (1), p.5-16 |
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| container_title | Cardiovascular drugs and therapy |
| container_volume | 27 |
| creator | Whittington, Hannah J. Hall, Andrew R. McLaughlin, Catarina P. Hausenloy, Derek J. Yellon, Derek M. Mocanu, Mihaela M. |
| description | Purpose
Clinical and experimental investigations demonstrated that metformin, a widely used anti-diabetic drug, exhibits cardioprotective properties against myocardial infarction. Interestingly, metformin was previously shown to increase the expression of PGC-1α a key controller of energy metabolism in skeletal muscle, which is down-regulated in diabetic conditions. We hypothesized that chronic treatment with metformin could protect the aged, diabetic heart against ischemia-reperfusion injury (IRI) by up-regulating PGC-1α and improving the impaired functionality of diabetic mitochondria.
Methods
Following 4 weeks of metformin (300 mg/kg) administered in the drinking water, 12 month-old diabetic Goto Kakizaki and non-diabetic Wistar rat hearts were assigned for infarct measurement following 35 min ischemia and 60 min reperfusion or for electron microscopy (EM) and Western blotting (WB) investigations.
Results
Metformin elicited a cardioprotective effect in both non-diabetic and diabetic hearts. In contrast with the diabetic non-treated hearts, the diabetic hearts treated with metformin showed more organized and elongated mitochondria and demonstrated a significant increase in phosphorylated AMPK and in PGC-1α expression.
Conclusions
In summary these results show for the first time that chronic metformin treatment augments myocardial resistance to ischemia-reperfusion injury, by an alternative mechanism in addition to the lowering of blood glucose. This consisted of a positive effect on mitochondrial structure possibly via a pathway involving AMPK activation and PGC-1α. Thus, metformin prescribed chronically to patients may lead to a basal state of cardioprotection thereby potentially limiting the occurrence of myocardial damage by cardiovascular events. |
| doi_str_mv | 10.1007/s10557-012-6425-x |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1282514758</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2874785851</sourcerecordid><originalsourceid>FETCH-LOGICAL-c445t-e81c7f265097cff02092ce363bfb572efea0b8a37467b65ce91f56c4346416723</originalsourceid><addsrcrecordid>eNp1kUtv1DAUhS1E1Q6lP6CbyhJC6iat7fiRsKtGtBRNgQWsLcdz3XGV2IOdiPLv6yHDQ5VYWJauv3N97j0InVJyQQlRl5kSIVRFKKskZ6J6fIEWVKi6UozTl2hBWkaqmhF5hF7l_ECKpm2bQ3TEatoy3qgF2iw3KQZv8R2MLqbBB3yVc7TejLDGS5PWPm5THMGOPpa3e-NDHvFtcCb9Kr3Dn-KIP06laPBNP9mYAa_iD0g-3OMvGwhxKCe8RgfO9BlO9vcx-nb9_uvyQ7X6fHO7vFpVlnMxVtBQqxyTgrTKOkdYmcFCLevOdUIxcGBI15hacak6KSy01Alpec0lp1Kx-hidz32L6-8T5FEPPlvoexMgTllT1jBBuRJNQd88Qx_ilEJxVyilFJVc8ELRmbIp5pzA6W3yg0k_NSV6F4OeY9AlBr2LQT8Wzdm-89QNsP6j-L33ArzdAyZb07tkgvX5L1fsNfM0bObydrdPSP9Y_O_vTwyLn9g</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1277716454</pqid></control><display><type>article</type><title>Chronic Metformin Associated Cardioprotection Against Infarction: Not Just a Glucose Lowering Phenomenon</title><source>Springer Link</source><creator>Whittington, Hannah J. ; Hall, Andrew R. ; McLaughlin, Catarina P. ; Hausenloy, Derek J. ; Yellon, Derek M. ; Mocanu, Mihaela M.</creator><creatorcontrib>Whittington, Hannah J. ; Hall, Andrew R. ; McLaughlin, Catarina P. ; Hausenloy, Derek J. ; Yellon, Derek M. ; Mocanu, Mihaela M.</creatorcontrib><description>Purpose
Clinical and experimental investigations demonstrated that metformin, a widely used anti-diabetic drug, exhibits cardioprotective properties against myocardial infarction. Interestingly, metformin was previously shown to increase the expression of PGC-1α a key controller of energy metabolism in skeletal muscle, which is down-regulated in diabetic conditions. We hypothesized that chronic treatment with metformin could protect the aged, diabetic heart against ischemia-reperfusion injury (IRI) by up-regulating PGC-1α and improving the impaired functionality of diabetic mitochondria.
Methods
Following 4 weeks of metformin (300 mg/kg) administered in the drinking water, 12 month-old diabetic Goto Kakizaki and non-diabetic Wistar rat hearts were assigned for infarct measurement following 35 min ischemia and 60 min reperfusion or for electron microscopy (EM) and Western blotting (WB) investigations.
Results
Metformin elicited a cardioprotective effect in both non-diabetic and diabetic hearts. In contrast with the diabetic non-treated hearts, the diabetic hearts treated with metformin showed more organized and elongated mitochondria and demonstrated a significant increase in phosphorylated AMPK and in PGC-1α expression.
Conclusions
In summary these results show for the first time that chronic metformin treatment augments myocardial resistance to ischemia-reperfusion injury, by an alternative mechanism in addition to the lowering of blood glucose. This consisted of a positive effect on mitochondrial structure possibly via a pathway involving AMPK activation and PGC-1α. Thus, metformin prescribed chronically to patients may lead to a basal state of cardioprotection thereby potentially limiting the occurrence of myocardial damage by cardiovascular events.</description><identifier>ISSN: 0920-3206</identifier><identifier>EISSN: 1573-7241</identifier><identifier>DOI: 10.1007/s10557-012-6425-x</identifier><identifier>PMID: 23192487</identifier><identifier>CODEN: CDTHET</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Aging - blood ; Aging - metabolism ; Aging - pathology ; Animals ; Biological and medical sciences ; Blood Glucose - metabolism ; Blotting, Western ; Cardiology ; Cardiology. Vascular system ; Cardiotonic Agents - administration & dosage ; Cardiotonic Agents - pharmacology ; Cardiotonic Agents - therapeutic use ; Cardiovascular system ; Diabetes Mellitus, Experimental - drug therapy ; Dose-Response Relationship, Drug ; Hypoglycemic Agents - administration & dosage ; Hypoglycemic Agents - pharmacology ; Hypoglycemic Agents - therapeutic use ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Metformin - administration & dosage ; Metformin - pharmacology ; Metformin - therapeutic use ; Microscopy, Electron ; Mitochondria, Heart - drug effects ; Mitochondria, Heart - ultrastructure ; Myocardial Infarction - drug therapy ; Myocardial Infarction - enzymology ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocardium - enzymology ; Myocardium - metabolism ; Myocardium - ultrastructure ; Original Article ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Pharmacology. Drug treatments ; Protein Kinases - metabolism ; Rats ; Rats, Wistar ; RNA-Binding Proteins - biosynthesis ; Transcription Factors - biosynthesis</subject><ispartof>Cardiovascular drugs and therapy, 2013-02, Vol.27 (1), p.5-16</ispartof><rights>Springer Science+Business Media New York 2012</rights><rights>2014 INIST-CNRS</rights><rights>Springer Science+Business Media New York 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c445t-e81c7f265097cff02092ce363bfb572efea0b8a37467b65ce91f56c4346416723</citedby><cites>FETCH-LOGICAL-c445t-e81c7f265097cff02092ce363bfb572efea0b8a37467b65ce91f56c4346416723</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27588672$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23192487$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Whittington, Hannah J.</creatorcontrib><creatorcontrib>Hall, Andrew R.</creatorcontrib><creatorcontrib>McLaughlin, Catarina P.</creatorcontrib><creatorcontrib>Hausenloy, Derek J.</creatorcontrib><creatorcontrib>Yellon, Derek M.</creatorcontrib><creatorcontrib>Mocanu, Mihaela M.</creatorcontrib><title>Chronic Metformin Associated Cardioprotection Against Infarction: Not Just a Glucose Lowering Phenomenon</title><title>Cardiovascular drugs and therapy</title><addtitle>Cardiovasc Drugs Ther</addtitle><addtitle>Cardiovasc Drugs Ther</addtitle><description>Purpose
Clinical and experimental investigations demonstrated that metformin, a widely used anti-diabetic drug, exhibits cardioprotective properties against myocardial infarction. Interestingly, metformin was previously shown to increase the expression of PGC-1α a key controller of energy metabolism in skeletal muscle, which is down-regulated in diabetic conditions. We hypothesized that chronic treatment with metformin could protect the aged, diabetic heart against ischemia-reperfusion injury (IRI) by up-regulating PGC-1α and improving the impaired functionality of diabetic mitochondria.
Methods
Following 4 weeks of metformin (300 mg/kg) administered in the drinking water, 12 month-old diabetic Goto Kakizaki and non-diabetic Wistar rat hearts were assigned for infarct measurement following 35 min ischemia and 60 min reperfusion or for electron microscopy (EM) and Western blotting (WB) investigations.
Results
Metformin elicited a cardioprotective effect in both non-diabetic and diabetic hearts. In contrast with the diabetic non-treated hearts, the diabetic hearts treated with metformin showed more organized and elongated mitochondria and demonstrated a significant increase in phosphorylated AMPK and in PGC-1α expression.
Conclusions
In summary these results show for the first time that chronic metformin treatment augments myocardial resistance to ischemia-reperfusion injury, by an alternative mechanism in addition to the lowering of blood glucose. This consisted of a positive effect on mitochondrial structure possibly via a pathway involving AMPK activation and PGC-1α. Thus, metformin prescribed chronically to patients may lead to a basal state of cardioprotection thereby potentially limiting the occurrence of myocardial damage by cardiovascular events.</description><subject>Aging - blood</subject><subject>Aging - metabolism</subject><subject>Aging - pathology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - metabolism</subject><subject>Blotting, Western</subject><subject>Cardiology</subject><subject>Cardiology. Vascular system</subject><subject>Cardiotonic Agents - administration & dosage</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Cardiotonic Agents - therapeutic use</subject><subject>Cardiovascular system</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Dose-Response Relationship, Drug</subject><subject>Hypoglycemic Agents - administration & dosage</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metformin - administration & dosage</subject><subject>Metformin - pharmacology</subject><subject>Metformin - therapeutic use</subject><subject>Microscopy, Electron</subject><subject>Mitochondria, Heart - drug effects</subject><subject>Mitochondria, Heart - ultrastructure</subject><subject>Myocardial Infarction - drug therapy</subject><subject>Myocardial Infarction - enzymology</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardium - enzymology</subject><subject>Myocardium - metabolism</subject><subject>Myocardium - ultrastructure</subject><subject>Original Article</subject><subject>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha</subject><subject>Pharmacology. Drug treatments</subject><subject>Protein Kinases - metabolism</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>RNA-Binding Proteins - biosynthesis</subject><subject>Transcription Factors - biosynthesis</subject><issn>0920-3206</issn><issn>1573-7241</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNp1kUtv1DAUhS1E1Q6lP6CbyhJC6iat7fiRsKtGtBRNgQWsLcdz3XGV2IOdiPLv6yHDQ5VYWJauv3N97j0InVJyQQlRl5kSIVRFKKskZ6J6fIEWVKi6UozTl2hBWkaqmhF5hF7l_ECKpm2bQ3TEatoy3qgF2iw3KQZv8R2MLqbBB3yVc7TejLDGS5PWPm5THMGOPpa3e-NDHvFtcCb9Kr3Dn-KIP06laPBNP9mYAa_iD0g-3OMvGwhxKCe8RgfO9BlO9vcx-nb9_uvyQ7X6fHO7vFpVlnMxVtBQqxyTgrTKOkdYmcFCLevOdUIxcGBI15hacak6KSy01Alpec0lp1Kx-hidz32L6-8T5FEPPlvoexMgTllT1jBBuRJNQd88Qx_ilEJxVyilFJVc8ELRmbIp5pzA6W3yg0k_NSV6F4OeY9AlBr2LQT8Wzdm-89QNsP6j-L33ArzdAyZb07tkgvX5L1fsNfM0bObydrdPSP9Y_O_vTwyLn9g</recordid><startdate>20130201</startdate><enddate>20130201</enddate><creator>Whittington, Hannah J.</creator><creator>Hall, Andrew R.</creator><creator>McLaughlin, Catarina P.</creator><creator>Hausenloy, Derek J.</creator><creator>Yellon, Derek M.</creator><creator>Mocanu, Mihaela M.</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</general><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7Z</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20130201</creationdate><title>Chronic Metformin Associated Cardioprotection Against Infarction: Not Just a Glucose Lowering Phenomenon</title><author>Whittington, Hannah J. ; Hall, Andrew R. ; McLaughlin, Catarina P. ; Hausenloy, Derek J. ; Yellon, Derek M. ; Mocanu, Mihaela M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c445t-e81c7f265097cff02092ce363bfb572efea0b8a37467b65ce91f56c4346416723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Aging - blood</topic><topic>Aging - metabolism</topic><topic>Aging - pathology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - metabolism</topic><topic>Blotting, Western</topic><topic>Cardiology</topic><topic>Cardiology. Vascular system</topic><topic>Cardiotonic Agents - administration & dosage</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Cardiotonic Agents - therapeutic use</topic><topic>Cardiovascular system</topic><topic>Diabetes Mellitus, Experimental - drug therapy</topic><topic>Dose-Response Relationship, Drug</topic><topic>Hypoglycemic Agents - administration & dosage</topic><topic>Hypoglycemic Agents - pharmacology</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metformin - administration & dosage</topic><topic>Metformin - pharmacology</topic><topic>Metformin - therapeutic use</topic><topic>Microscopy, Electron</topic><topic>Mitochondria, Heart - drug effects</topic><topic>Mitochondria, Heart - ultrastructure</topic><topic>Myocardial Infarction - drug therapy</topic><topic>Myocardial Infarction - enzymology</topic><topic>Myocardial Infarction - metabolism</topic><topic>Myocardial Infarction - pathology</topic><topic>Myocardium - enzymology</topic><topic>Myocardium - metabolism</topic><topic>Myocardium - ultrastructure</topic><topic>Original Article</topic><topic>Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha</topic><topic>Pharmacology. Drug treatments</topic><topic>Protein Kinases - metabolism</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>RNA-Binding Proteins - biosynthesis</topic><topic>Transcription Factors - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Whittington, Hannah J.</creatorcontrib><creatorcontrib>Hall, Andrew R.</creatorcontrib><creatorcontrib>McLaughlin, Catarina P.</creatorcontrib><creatorcontrib>Hausenloy, Derek J.</creatorcontrib><creatorcontrib>Yellon, Derek M.</creatorcontrib><creatorcontrib>Mocanu, Mihaela M.</creatorcontrib><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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection (Proquest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research 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)</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Biochemistry Abstracts 1</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><collection>MEDLINE - Academic</collection><jtitle>Cardiovascular drugs and therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Whittington, Hannah J.</au><au>Hall, Andrew R.</au><au>McLaughlin, Catarina P.</au><au>Hausenloy, Derek J.</au><au>Yellon, Derek M.</au><au>Mocanu, Mihaela M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chronic Metformin Associated Cardioprotection Against Infarction: Not Just a Glucose Lowering Phenomenon</atitle><jtitle>Cardiovascular drugs and therapy</jtitle><stitle>Cardiovasc Drugs Ther</stitle><addtitle>Cardiovasc Drugs Ther</addtitle><date>2013-02-01</date><risdate>2013</risdate><volume>27</volume><issue>1</issue><spage>5</spage><epage>16</epage><pages>5-16</pages><issn>0920-3206</issn><eissn>1573-7241</eissn><coden>CDTHET</coden><abstract>Purpose
Clinical and experimental investigations demonstrated that metformin, a widely used anti-diabetic drug, exhibits cardioprotective properties against myocardial infarction. Interestingly, metformin was previously shown to increase the expression of PGC-1α a key controller of energy metabolism in skeletal muscle, which is down-regulated in diabetic conditions. We hypothesized that chronic treatment with metformin could protect the aged, diabetic heart against ischemia-reperfusion injury (IRI) by up-regulating PGC-1α and improving the impaired functionality of diabetic mitochondria.
Methods
Following 4 weeks of metformin (300 mg/kg) administered in the drinking water, 12 month-old diabetic Goto Kakizaki and non-diabetic Wistar rat hearts were assigned for infarct measurement following 35 min ischemia and 60 min reperfusion or for electron microscopy (EM) and Western blotting (WB) investigations.
Results
Metformin elicited a cardioprotective effect in both non-diabetic and diabetic hearts. In contrast with the diabetic non-treated hearts, the diabetic hearts treated with metformin showed more organized and elongated mitochondria and demonstrated a significant increase in phosphorylated AMPK and in PGC-1α expression.
Conclusions
In summary these results show for the first time that chronic metformin treatment augments myocardial resistance to ischemia-reperfusion injury, by an alternative mechanism in addition to the lowering of blood glucose. This consisted of a positive effect on mitochondrial structure possibly via a pathway involving AMPK activation and PGC-1α. Thus, metformin prescribed chronically to patients may lead to a basal state of cardioprotection thereby potentially limiting the occurrence of myocardial damage by cardiovascular events.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>23192487</pmid><doi>10.1007/s10557-012-6425-x</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aging - blood Aging - metabolism Aging - pathology Animals Biological and medical sciences Blood Glucose - metabolism Blotting, Western Cardiology Cardiology. Vascular system Cardiotonic Agents - administration & dosage Cardiotonic Agents - pharmacology Cardiotonic Agents - therapeutic use Cardiovascular system Diabetes Mellitus, Experimental - drug therapy Dose-Response Relationship, Drug Hypoglycemic Agents - administration & dosage Hypoglycemic Agents - pharmacology Hypoglycemic Agents - therapeutic use Male Medical sciences Medicine Medicine & Public Health Metformin - administration & dosage Metformin - pharmacology Metformin - therapeutic use Microscopy, Electron Mitochondria, Heart - drug effects Mitochondria, Heart - ultrastructure Myocardial Infarction - drug therapy Myocardial Infarction - enzymology Myocardial Infarction - metabolism Myocardial Infarction - pathology Myocardium - enzymology Myocardium - metabolism Myocardium - ultrastructure Original Article Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha Pharmacology. Drug treatments Protein Kinases - metabolism Rats Rats, Wistar RNA-Binding Proteins - biosynthesis Transcription Factors - biosynthesis |
| title | Chronic Metformin Associated Cardioprotection Against Infarction: Not Just a Glucose Lowering Phenomenon |
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