Acute induction of autophagy as a novel strategy for cardioprotection: Getting to the heart of the matter
There is no question that necrosis and apoptosis contribute to cardiomyocyte death in the setting of myocardial ischemia-reperfusion. Indeed, considerable effort and resources have been invested in the development of novel therapies aimed at attenuating necrotic and apoptotic cell death, with the ul...
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| Veröffentlicht in: | Autophagy 2011-04, Vol.7 (4), p.432-433 |
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| container_title | Autophagy |
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| creator | Przyklenk, Karin Reddy Undyala, Vishnu Vardhan Wider, Joseph Sala-Mercado, Javier A. Gottlieb, Roberta A Mentzer, Jr, Robert M. |
| description | There is no question that necrosis and apoptosis contribute to cardiomyocyte death in the setting of myocardial ischemia-reperfusion. Indeed, considerable effort and resources have been invested in the development of novel therapies aimed at attenuating necrotic and apoptotic cell death, with the ultimate goal of applying these strategies to reduce infarct size and improve outcome in patients suffering acute myocardial infarction (MI) or 'heart attack'. However, an issue that remains controversial is the role of autophagy in determining the fate of ischemic-reperfused cardiomyocytes: i.e., is induction of autophagy detrimental or protective? Recent data from our group obtained in the clinically relevant, in vivo swine model of acute MI provide novel evidence of a positive association between pharmacological upregulation of autophagy (achieved by administration of chloramphenicol succinate (CAPS)) and increased resistance to myocardial ischemia-reperfusion injury. |
| doi_str_mv | 10.4161/auto.7.4.14395 |
| format | Article |
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Indeed, considerable effort and resources have been invested in the development of novel therapies aimed at attenuating necrotic and apoptotic cell death, with the ultimate goal of applying these strategies to reduce infarct size and improve outcome in patients suffering acute myocardial infarction (MI) or 'heart attack'. However, an issue that remains controversial is the role of autophagy in determining the fate of ischemic-reperfused cardiomyocytes: i.e., is induction of autophagy detrimental or protective? Recent data from our group obtained in the clinically relevant, in vivo swine model of acute MI provide novel evidence of a positive association between pharmacological upregulation of autophagy (achieved by administration of chloramphenicol succinate (CAPS)) and increased resistance to myocardial ischemia-reperfusion injury.</description><identifier>ISSN: 1554-8627</identifier><identifier>EISSN: 1554-8635</identifier><identifier>DOI: 10.4161/auto.7.4.14395</identifier><identifier>PMID: 21187719</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>Animals ; Apoptosis ; Autophagic Punctum ; Autophagy ; Binding ; Biology ; Bioscience ; Calcium ; Cancer ; Cell ; chloramphenicol ; Chloramphenicol - analogs & derivatives ; Chloramphenicol - pharmacology ; Cycle ; Disease Models, Animal ; ischemia-reperfusion injury ; Landes ; Models, Biological ; myocardial infarction ; myocardial ischemia ; Myocardial Reperfusion Injury - pathology ; Myocardium - metabolism ; Myocytes, Cardiac - cytology ; Necrosis - metabolism ; Organogenesis ; Phenotype ; Phosphatidylinositol 3-Kinases - metabolism ; Proteins ; Signal Transduction ; Swine ; Time Factors</subject><ispartof>Autophagy, 2011-04, Vol.7 (4), p.432-433</ispartof><rights>Copyright © 2011 Landes Bioscience 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3679089/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3679089/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21187719$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Przyklenk, Karin</creatorcontrib><creatorcontrib>Reddy Undyala, Vishnu Vardhan</creatorcontrib><creatorcontrib>Wider, Joseph</creatorcontrib><creatorcontrib>Sala-Mercado, Javier A.</creatorcontrib><creatorcontrib>Gottlieb, Roberta A</creatorcontrib><creatorcontrib>Mentzer, Jr, Robert M.</creatorcontrib><title>Acute induction of autophagy as a novel strategy for cardioprotection: Getting to the heart of the matter</title><title>Autophagy</title><addtitle>Autophagy</addtitle><description>There is no question that necrosis and apoptosis contribute to cardiomyocyte death in the setting of myocardial ischemia-reperfusion. 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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Animals Apoptosis Autophagic Punctum Autophagy Binding Biology Bioscience Calcium Cancer Cell chloramphenicol Chloramphenicol - analogs & derivatives Chloramphenicol - pharmacology Cycle Disease Models, Animal ischemia-reperfusion injury Landes Models, Biological myocardial infarction myocardial ischemia Myocardial Reperfusion Injury - pathology Myocardium - metabolism Myocytes, Cardiac - cytology Necrosis - metabolism Organogenesis Phenotype Phosphatidylinositol 3-Kinases - metabolism Proteins Signal Transduction Swine Time Factors |
| title | Acute induction of autophagy as a novel strategy for cardioprotection: Getting to the heart of the matter |
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