| Mitochondrial adenine nucleotide transport and cardioprotection. | |
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MedLine Citation:
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PMID: 21945520 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Mitochondria are highly metabolically active cell organelles that not only act as the powerhouse of the cell by supplying energy through ATP production, but also play a destructive role by initiating cell death pathways. Growing evidence recognizes that mitochondrial dysfunction is one of the major causes of cardiovascular disease. Under de-energized conditions, slowing of adenine nucleotide transport in and out of the mitochondria significantly attenuates myocardial ischemia-reperfusion injury. The purpose of this review is to elaborate on and update the mechanistic pathways which may explain how altered adenine nucleotide transport can influence cardiovascular function. This article is part of a Special Issue entitled "Local Signaling in Myocytes". |
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Authors:
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Samarjit Das; Charles Steenbergen |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review Date: 2011-09-17 |
Journal Detail:
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Title: Journal of molecular and cellular cardiology Volume: 52 ISSN: 1095-8584 ISO Abbreviation: J. Mol. Cell. Cardiol. Publication Date: 2012 Feb |
Date Detail:
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Created Date: 2012-01-23 Completed Date: 2012-05-15 Revised Date: 2013-04-08 |
Medline Journal Info:
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Nlm Unique ID: 0262322 Medline TA: J Mol Cell Cardiol Country: England |
Other Details:
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Languages: eng Pagination: 448-53 Citation Subset: IM |
Copyright Information:
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Copyright © 2011 Elsevier Ltd. All rights reserved. |
Affiliation:
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Department of Pathology, Johns Hopkins University, Baltimore, MD, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenine Nucleotides
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metabolism*,
pharmacology* Animals Biological Transport Cardiotonic Agents / metabolism*, pharmacology* Glycogen Synthase Kinases / metabolism Humans Mitochondria, Heart / metabolism* Mitochondrial Membrane Transport Proteins / metabolism Myocardial Reperfusion Injury / metabolism*, prevention & control* Proto-Oncogene Proteins c-bcl-2 / metabolism Voltage-Dependent Anion Channels / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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R01 HL039752-25/HL/NHLBI NIH HHS; R01 HL39752/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Adenine Nucleotides; 0/Cardiotonic Agents; 0/Mitochondrial Membrane Transport Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/Voltage-Dependent Anion Channels; 0/mitochondrial permeability transition pore; EC 2.7.11.-/Glycogen Synthase Kinases |
| Comments/Corrections | |
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