Subcellular proteomics combined with bioenergetic phenotyping reveals protein biomarkers of respiratory insufficiency in the setting of proofreading-deficient mitochondrial polymerase

The mitochondrial mutator mouse is a well-established model of premature aging. In addition to accelerated aging, these mice develop hypertrophic cardiomyopathy at ~13 months of age, presumably due to overt mitochondrial dysfunction. Despite evidence of bioenergetic disruption within heart mitochond...

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Veröffentlicht in:	Scientific reports 2020-02, Vol.10 (1), p.3603-3603, Article 3603
Hauptverfasser:	McLaughlin, Kelsey L., Kew, Kimberly A., McClung, Joseph M., Fisher-Wellman, Kelsey H.
Format:	Artikel
Sprache:	eng
Schlagworte:	631/443/319/333 631/443/319/333/1465 631/443/7 631/45/475 Aging Aging, Premature - genetics Animals Bioenergetics Biomarkers Biomarkers - metabolism Cardiomyopathy Cardiomyopathy, Hypertrophic - genetics Cardiomyopathy, Hypertrophic - metabolism Conductance Disease Models, Animal DNA Polymerase gamma - genetics Electron Transport Complex I - metabolism Energy Metabolism Humanities and Social Sciences Humans Mice Mice, Inbred C57BL Mitochondria Mitochondria, Heart - genetics Mitochondria, Heart - metabolism Mitochondrial DNA multidisciplinary Mutation - genetics Phenotype Phenotyping Proofreading Proteins Proteomes Proteomics Respiratory function Respiratory Insufficiency - genetics Respiratory Insufficiency - metabolism Science Science (multidisciplinary) Skeletal muscle Subcellular Fractions - metabolism
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