Document Detail


Mitochondria and mitophagy: the yin and yang of cell death control.
MedLine Citation:
PMID:  23065344     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Mitochondria are primarily responsible for providing the contracting cardiac myocyte with a continuous supply of ATP. However, mitochondria can rapidly change into death-promoting organelles. In response to changes in the intracellular environment, mitochondria become producers of excessive reactive oxygen species and release prodeath proteins, resulting in disrupted ATP synthesis and activation of cell death pathways. Interestingly, cells have developed a defense mechanism against aberrant mitochondria that can cause harm to the cell. This mechanism involves selective sequestration and subsequent degradation of the dysfunctional mitochondrion before it causes activation of cell death. Induction of mitochondrial autophagy, or mitophagy, results in selective clearance of damaged mitochondria in cells. In response to stress such as ischemia/reperfusion, prosurvival and prodeath pathways are concomitantly activated in cardiac myocytes. Thus, there is a delicate balance between life and death in the myocytes during stress, and the final outcome depends on the complex cross-talk between these pathways. Mitophagy functions as an early cardioprotective response, favoring adaptation to stress by removing damaged mitochondria. In contrast, increased oxidative stress and apoptotic proteases can inactivate mitophagy, allowing for the execution of cell death. Herein, we discuss the importance of mitochondria and mitophagy in cardiovascular health and disease and provide a review of our current understanding of how these processes are regulated.
Authors:
Dieter A Kubli; Åsa B Gustafsson
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Circulation research     Volume:  111     ISSN:  1524-4571     ISO Abbreviation:  Circ. Res.     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-10-15     Completed Date:  2013-01-31     Revised Date:  2013-10-17    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1208-21     Citation Subset:  IM    
Affiliation:
Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, CA 92093, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / metabolism
Animals
Apoptosis / physiology*
Humans
Mitochondria, Heart / physiology*
Mitochondrial Degradation / physiology*
Myocytes, Cardiac / cytology,  physiology*
Oxidative Stress / physiology
Reactive Oxygen Species / metabolism
Grant Support
ID/Acronym/Agency:
R01 HL087023/HL/NHLBI NIH HHS; R01 HL101217/HL/NHLBI NIH HHS; R01HL087023/HL/NHLBI NIH HHS; R01HL092136/HL/NHLBI NIH HHS; R01HL101217/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Reactive Oxygen Species; 56-65-5/Adenosine Triphosphate
Comments/Corrections

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