Source:http://linkedlifedata.com/resource/pubmed/id/11389925
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
2001-6-6
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pubmed:abstractText |
In senescence, endogenous mechanisms of cardioprotection are apparently attenuated resulting in increased vulnerability to ischemia-reperfusion. In particular, mitochondria, which are essential in maintaining cardiac energetic and ionic homeostasis, are susceptible to Ca2+ overload, a component of metabolic injury. However, effective means of protecting senescent mitochondria are lacking. Here, mitochondrial function and structure were assessed using ion-selective mini-electrodes, high-performance liquid chromatography and electron microscopy. Aging decreased ADP-induced oxygen consumption and prolonged the time associated with ADP to ATP conversion, which manifested as a reduced rate of oxidative phosphorylation. Aging also reduced mitochondrial Ca2+ handling, and increased Ca2+-induced mitochondrial damage. Diazoxide, a potassium channel opener, reduced Ca2+ loading and protected the functional and structural integrity of senescent mitochondria from Ca2+-induced injury. In this way, the present study identifies the potential usefulness for pharmacotherapy in protecting vulnerable senescent mitochondria from conditions of Ca2+ overload, such as ischemia-reperfusion.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0047-6374
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
31
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pubmed:volume |
122
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1073-86
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11389925-Aging,
pubmed-meshheading:11389925-Animals,
pubmed-meshheading:11389925-Calcium,
pubmed-meshheading:11389925-Diazoxide,
pubmed-meshheading:11389925-Ion Channel Gating,
pubmed-meshheading:11389925-Mitochondria, Heart,
pubmed-meshheading:11389925-Myocardium,
pubmed-meshheading:11389925-Oxidation-Reduction,
pubmed-meshheading:11389925-Phosphorylation,
pubmed-meshheading:11389925-Potassium Channels,
pubmed-meshheading:11389925-Rats,
pubmed-meshheading:11389925-Rats, Inbred F344
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pubmed:year |
2001
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pubmed:articleTitle |
Increased calcium vulnerability of senescent cardiac mitochondria: protective role for a mitochondrial potassium channel opener.
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pubmed:affiliation |
Division of Cardiovascular Diseases, Departments of Medicine, Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Mayo Foundation, Guggenheim 7, Rochester, MN 55905, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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