Abstract:
:Mitochondrial dysfunction is an underlying cause of ischemia-reperfusion injury. In particular, ischemic injury induces dramatic increases in mitochondrial permeability, thereby instigating a chain of events that leads to both apoptotic and necrotic cardiomyocyte death. The mitochondrial permeability transition (MPT) pore, a large, non-specific channel that spans the inner mitochondrial membrane, is known to mediate the lethal permeability changes that initiate mitochondrial-driven cardiomyocyte death. The purpose of this review is to focus on the role of the MPT pore in ischemia-reperfusion injury, the mechanisms involved, and, in particular, what we do and do not know regarding the pore's molecular composition.
journal_name
Basic Res Cardioljournal_title
Basic research in cardiologyauthors
Baines CPdoi
10.1007/s00395-009-0004-8subject
Has Abstractpub_date
2009-03-01 00:00:00pages
181-8issue
2eissn
0300-8428issn
1435-1803journal_volume
104pub_type
杂志文章,评审abstract::Alcoholic heart muscle disease is characterized by structural changes which include chamber dilation, ventricular hypertrophy, and myocyte damage. These effects often lead to contractile dysfunction and ultimately to heart failure if alcohol consumption is not terminated. In rat models for heart failure in which heart...
journal_title:Basic research in cardiology
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journal_title:Basic research in cardiology
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pub_type: 杂志文章,评审
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journal_title:Basic research in cardiology
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doi:10.1007/BF01907225
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journal_title:Basic research in cardiology
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journal_title:Basic research in cardiology
pub_type: 杂志文章
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journal_title:Basic research in cardiology
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journal_title:Basic research in cardiology
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journal_title:Basic research in cardiology
pub_type: 杂志文章,评审
doi:
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journal_title:Basic research in cardiology
pub_type: 杂志文章,评审
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