Document Detail


What makes the mitochondria a killer? Can we condition them to be less destructive?
MedLine Citation:
PMID:  20837069     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Cardioprotection, such as preconditioning and postconditioning, has been shown to result in a significant reduction in cell death. Many of the signaling pathways activated by cardioprotection have been elucidated, but there is still a lack of understanding of the mechanisms by which these signaling pathways reduce cell death. Mitochondria have been reported to be an important player in many types of apoptotic and necrotic cell death. If mitochondria play an important role in cell death, then it seems reasonable to consider that cardioprotective mechanisms might act, at least in part, by opposing mitochondrial cell death pathways. One of the major mechanisms of cell death in ischemia-reperfusion is suggested to be the opening of a large conductance pore in the inner mitochondrial membrane, known as the mitochondrial permeability transition pore. Inhibition of this mitochondrial pore appears to be one of the major mechanisms by which cardioprotection reduces cell death. Cardioprotection activates a number of signaling pathways that reduce the level of triggers (reactive oxygen species and calcium) or enhances inhibitors of the mitochondrial permeability transition pore at the start of reperfusion. This article is part of a Special Issue entitled: Mitochondria and Cardioprotection.
Authors:
Elizabeth Murphy; Charles Steenbergen
Related Documents :
21059189 - Analysis of the rpn11-m1 proteasomal mutant reveals connection between cell cycle and m...
17289009 - Different mechanisms involved in apoptosis following exposure to benzo[a]pyrene in f258...
22901079 - Roles of cell walls and intracellular contents in supercooling capability of xylem pare...
12588799 - Parkin prevents mitochondrial swelling and cytochrome c release in mitochondria-depende...
22531009 - Sertoli cell quiescence - new insights.
16949859 - Study the oxidative injury of yeast cells by nadh autofluorescence.
19709579 - Supercritical carbon dioxide extract of physalis peruviana induced cell cycle arrest an...
19631359 - Human intervertebral disc-derived cells are recruited by human serum and form nucleus p...
11895859 - Apoptosis of squamous cells at different stages of carcinogenesis following 4-hpr treat...
Publication Detail:
Type:  Journal Article; Review     Date:  2010-09-15
Journal Detail:
Title:  Biochimica et biophysica acta     Volume:  1813     ISSN:  0006-3002     ISO Abbreviation:  Biochim. Biophys. Acta     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-06-06     Completed Date:  2011-08-05     Revised Date:  2013-03-05    
Medline Journal Info:
Nlm Unique ID:  0217513     Medline TA:  Biochim Biophys Acta     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  1302-8     Citation Subset:  IM    
Copyright Information:
Copyright © 2010. Published by Elsevier B.V.
Affiliation:
Translational Medicine Branch, NHLBI, NIH, Bethesda, MD 20892, USA. murphy1@nhlbi.nih.gov
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Calcium / metabolism
Cell Death
Ischemic Preconditioning, Myocardial
Mice
Mitochondria, Heart / metabolism*
Mitochondrial Membrane Transport Proteins / metabolism*
Myocardial Reperfusion Injury / metabolism*,  pathology
Myocytes, Cardiac / physiology*
Reactive Oxygen Species / metabolism
Signal Transduction
Grant Support
ID/Acronym/Agency:
R01 HL039752/HL/NHLBI NIH HHS; ZIA HL002065-04/HL/NHLBI NIH HHS; ZIA HL002066-04/HL/NHLBI NIH HHS; ZIA HL006059-02/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Mitochondrial Membrane Transport Proteins; 0/Reactive Oxygen Species; 0/mitochondrial permeability transition pore; 7440-70-2/Calcium
Comments/Corrections

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


Previous Document:  Cage-induced stereotypies in female ICR CD-1 mice do not correlate with recurrent perseveration.
Next Document:  GP4-specific neutralizing antibodies might be a driving force in PRRSV evolution.