Document Detail


Mitochondrial adenine nucleotide transport and cardioprotection.
MedLine Citation:
PMID:  21945520     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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".
Authors:
Samarjit Das; Charles Steenbergen
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2011-09-17
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  52     ISSN:  1095-8584     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-01-23     Completed Date:  2012-05-15     Revised Date:  2014-09-18    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  448-53     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Ltd. All rights reserved.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Adenine Nucleotides / 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:
R01 HL039752/HL/NHLBI NIH HHS; R01 HL039752-25/HL/NHLBI NIH HHS; R01 HL39752/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
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

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Ontogenic changes in placental transthyretin.
Next Document:  Redox modification of cell signaling in the cardiovascular system.