Document Detail


Mitochondrial membrane permeabilization and cell death during myocardial infarction: roles of calcium and reactive oxygen species.
MedLine Citation:
PMID:  23176689     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Excess generation of reactive oxygen species (ROS) and cytosolic calcium accumulation play major roles in the initiation of programmed cell death during acute myocardial infarction. Cell death may include necrosis, apoptosis and autophagy, and combinations thereof. During ischemia, calcium handling between the sarcoplasmic reticulum and myofilament is disrupted and calcium is diverted to the mitochondria causing swelling. Reperfusion, while essential for survival, reactivates energy transduction and contractility and causes the release of ROS and additional ionic imbalance. During acute ischemia-reperfusion, the principal death pathways are programmed necrosis and apoptosis through the intrinsic pathway, initiated by the opening of the mitochondrial permeability transition pore and outer mitochondrial membrane permeabilization, respectively. Despite intense investigation, the mechanisms of action and modes of regulation of mitochondrial membrane permeabilization are incompletely understood. Extrinsic apoptosis, necroptosis and autophagy may also contribute to ischemia-reperfusion injury. In this review, the roles of dysregulated calcium and ROS and the contributions of Bcl-2 proteins, as well as mitochondrial morphology in promoting mitochondrial membrane permeability change and the ensuing cell death during myocardial infarction are discussed.
Authors:
Keith A Webster
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Future cardiology     Volume:  8     ISSN:  1744-8298     ISO Abbreviation:  Future Cardiol     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-11-26     Completed Date:  2013-05-06     Revised Date:  2013-09-03    
Medline Journal Info:
Nlm Unique ID:  101239345     Medline TA:  Future Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  863-84     Citation Subset:  IM    
Affiliation:
Department of Molecular & Cellular Pharmacology, University of Miami Medical Center, FL 33101, USA. kwebster@med.miami.edu
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MeSH Terms
Descriptor/Qualifier:
Apoptosis / physiology
Calcium / analysis,  physiology*
Cell Death / physiology
Cytosol / chemistry
Humans
Mitochondrial Membranes / physiology*
Myocardial Infarction / physiopathology*
Permeability
Reactive Oxygen Species*
Grant Support
ID/Acronym/Agency:
HL44578/HL/NHLBI NIH HHS; R01 HL044578/HL/NHLBI NIH HHS; R01 HL072924/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Reactive Oxygen Species; 7440-70-2/Calcium
Comments/Corrections

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


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