| pubmed-article:16909385 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16909385 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:16909385 | lifeskim:mentions | umls-concept:C0001792 | lld:lifeskim |
| pubmed-article:16909385 | lifeskim:mentions | umls-concept:C1704336 | lld:lifeskim |
| pubmed-article:16909385 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
| pubmed-article:16909385 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
| pubmed-article:16909385 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
| pubmed-article:16909385 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:16909385 | pubmed:dateCreated | 2006-8-15 | lld:pubmed |
| pubmed-article:16909385 | pubmed:abstractText | Skeletal muscle-mass loss with age has severe health consequences, yet the molecular basis of the loss remains obscure. Although mitochondrial DNA (mtDNA)-deletion mutations have been shown to accumulate with age, for these aberrant genomes to be physiologically relevant, they must accumulate to high levels intracellularly and be present in a significant number of cells. We examined mtDNA-deletion mutations in vastus lateralis (VL) muscle of human subjects aged 49-93 years, using both histologic and polymerase-chain-reaction (PCR) analyses, to determine the physiological and genomic integrity of mitochondria in aging human muscle. The number of VL muscle fibers exhibiting mitochondrial electron-transport-system (ETS) abnormalities increased from an estimated 6% at age 49 years to 31% at age 92 years. We analyzed the mitochondrial genotype of 48 single ETS-abnormal, cytochrome c oxidase-negative/succinate dehydrogenase-hyperreactive (COX-/SDH++) fibers from normal aging human subjects and identified mtDNA-deletion mutations in all abnormal fibers. Deletion mutations were clonal within a fiber and concomitant to the COX-/SDH++ region. Quantitative PCR analysis of wild-type and deletion-containing mtDNA genomes within ETS-abnormal regions of single fibers demonstrated that these deletion mutations accumulate to detrimental levels (>90% of the total mtDNA). | lld:pubmed |
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| pubmed-article:16909385 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16909385 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16909385 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16909385 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16909385 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:16909385 | pubmed:issn | 0002-9297 | lld:pubmed |
| pubmed-article:16909385 | pubmed:author | pubmed-author:AikenJudd MJM | lld:pubmed |
| pubmed-article:16909385 | pubmed:author | pubmed-author:BuaEntelaE | lld:pubmed |
| pubmed-article:16909385 | pubmed:author | pubmed-author:McKenzieDebbi... | lld:pubmed |
| pubmed-article:16909385 | pubmed:author | pubmed-author:HerbstAllenA | lld:pubmed |
| pubmed-article:16909385 | pubmed:author | pubmed-author:JohnsonJodyJ | lld:pubmed |
| pubmed-article:16909385 | pubmed:author | pubmed-author:SalamatShahri... | lld:pubmed |
| pubmed-article:16909385 | pubmed:author | pubmed-author:DelongBridget... | lld:pubmed |
| pubmed-article:16909385 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16909385 | pubmed:volume | 79 | lld:pubmed |
| pubmed-article:16909385 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16909385 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16909385 | pubmed:pagination | 469-80 | lld:pubmed |
| pubmed-article:16909385 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:16909385 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16909385 | pubmed:articleTitle | Mitochondrial DNA-deletion mutations accumulate intracellularly to detrimental levels in aged human skeletal muscle fibers. | lld:pubmed |
| pubmed-article:16909385 | pubmed:affiliation | Department of Animal Health and Biomedical Sciences, University of Wisconsin, Madison, WI 53706, USA. | lld:pubmed |
| pubmed-article:16909385 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16909385 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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