Integration of cellular bioenergetics with mitochondrial quality control and autophagy
Identifieur interne : 001388 ( Main/Exploration ); précédent : 001387; suivant : 001389Integration of cellular bioenergetics with mitochondrial quality control and autophagy
Auteurs : Bradford G. Hill ; Gloria A. Benavides ; Jack R. Lancaster ; Scott Ballinger ; Lou Dell Talia ; Jianhua Zhang ; Victor M. Darley-UsmarSource :
- Biological Chemistry [ 1431-6730 ] ; 2012.
English descriptors
- Teeft :
- Acad, Acta, Adipose, Assay, Atg7, Autophagy, Ballinger, Basal, Benavides, Biochem, Biochim, Bioenergetic, Bioenergetic dysfunction, Bioenergetic reserve capacity, Bioenergetics, Biogenesis, Biol, Biophys, Cardiomyocytes, Cardiovascular disease, Cell biol, Cell death, Cellular, Cellular bioenergetics, Chem, Clin, Dranka, Drp1, Dysfunction, Ecar, Endothelial cells, Extracellular, Fccp, Free radic, Genet, Genetics, Glucose, Glycolysis, Glycolytic, Haplotype, Hepatocytes, Hepatotoxicity, Kinase, Landar, Lc3ii, Leak, Lemasters, Lipid, Metabolic, Mitochondrial, Mitochondrial damage, Mitochondrial dysfunction, Mitochondrial function, Mitochondrial quality, Mitochondrial quality control, Mitochondrial reserve capacity, Mitochondrial respiration, Mitochondrion, Mitophagic, Mitophagy, Mtdna, Mtdna damage, Mutation, Narendra, Natl, Nicholls, Nitric, Nitric oxide, Oligomycin, Organelle, Oxidant, Oxidase, Oxidative, Oxidative phosphorylation, Oxidative stress, Oxygen consumption, Parkin, Pathway, Phosphorylation, Physiol, Pink1, Proc, Proton, Proton leak, Pyruvate, Reactive, Reserve capacity, Respiration, Sansbury, Sato, Skeletal muscle, Stateapparent, Substrate availability, Uncoupling, Wang, Youle, Zelickson, Zhang.
Abstract
Bioenergetic dysfunction is emerging as a cornerstone for establishing a framework for understanding the pathophysiology of cardiovascular disease, diabetes, cancer and neurodegeneration. Recent advances in cellular bioenergetics have shown that many cells maintain a substantial bioenergetic reserve capacity, which is a prospective index of ‘healthy’ mitochondrial populations. The bioenergetics of the cell are likely regulated by energy requirements and substrate availability. Additionally, the overall quality of the mitochondrial population and the relative abundance of mitochondria in cells and tissues also impinge on overall bioenergetic capacity and resistance to stress. Because mitochondria are susceptible to damage mediated by reactive oxygen/nitrogen and lipid species, maintaining a ‘healthy’ population of mitochondria through quality control mechanisms appears to be essential for cell survival under conditions of pathological stress. Accumulating evidence suggest that mitophagy is particularly important for preventing amplification of initial oxidative insults, which otherwise would further impair the respiratory chain or promote mutations in mitochondrial DNA (mtDNA). The processes underlying the regulation of mitophagy depend on several factors, including the integrity of mtDNA, electron transport chain activity, and the interaction and regulation of the autophagic machinery. The integration and interpretation of cellular bioenergetics in the context of mitochondrial quality control and genetics is the theme of this review.
Url:
DOI: 10.1515/hsz-2012-0198
Affiliations:
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Hill</name></author><author><name sortKey="Benavides, Gloria A" sort="Benavides, Gloria A" uniqKey="Benavides G" first="Gloria A." last="Benavides">Gloria A. Benavides</name></author><author><name sortKey="Lancaster, Jack R" sort="Lancaster, Jack R" uniqKey="Lancaster J" first="Jack R." last="Lancaster">Jack R. Lancaster</name></author><author><name sortKey="Ballinger, Scott" sort="Ballinger, Scott" uniqKey="Ballinger S" first="Scott" last="Ballinger">Scott Ballinger</name></author><author><name sortKey="Dell Talia, Lou" sort="Dell Talia, Lou" uniqKey="Dell Talia L" first="Lou" last="Dell Talia">Lou Dell Talia</name></author><author><name sortKey="Zhang, Jianhua" sort="Zhang, Jianhua" uniqKey="Zhang J" first="Jianhua" last="Zhang">Jianhua Zhang</name></author><author><name sortKey="Darley Usmar, Victor M" sort="Darley Usmar, Victor M" uniqKey="Darley Usmar V" first="Victor M." last="Darley-Usmar">Victor M. 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Recent advances in cellular bioenergetics have shown that many cells maintain a substantial bioenergetic reserve capacity, which is a prospective index of ‘healthy’ mitochondrial populations. The bioenergetics of the cell are likely regulated by energy requirements and substrate availability. Additionally, the overall quality of the mitochondrial population and the relative abundance of mitochondria in cells and tissues also impinge on overall bioenergetic capacity and resistance to stress. Because mitochondria are susceptible to damage mediated by reactive oxygen/nitrogen and lipid species, maintaining a ‘healthy’ population of mitochondria through quality control mechanisms appears to be essential for cell survival under conditions of pathological stress. Accumulating evidence suggest that mitophagy is particularly important for preventing amplification of initial oxidative insults, which otherwise would further impair the respiratory chain or promote mutations in mitochondrial DNA (mtDNA). The processes underlying the regulation of mitophagy depend on several factors, including the integrity of mtDNA, electron transport chain activity, and the interaction and regulation of the autophagic machinery. The integration and interpretation of cellular bioenergetics in the context of mitochondrial quality control and genetics is the theme of this review.</div></front></TEI><affiliations><list></list><tree><noCountry><name sortKey="Ballinger, Scott" sort="Ballinger, Scott" uniqKey="Ballinger S" first="Scott" last="Ballinger">Scott Ballinger</name><name sortKey="Benavides, Gloria A" sort="Benavides, Gloria A" uniqKey="Benavides G" first="Gloria A." last="Benavides">Gloria A. Benavides</name><name sortKey="Darley Usmar, Victor M" sort="Darley Usmar, Victor M" uniqKey="Darley Usmar V" first="Victor M." last="Darley-Usmar">Victor M. Darley-Usmar</name><name sortKey="Dell Talia, Lou" sort="Dell Talia, Lou" uniqKey="Dell Talia L" first="Lou" last="Dell Talia">Lou Dell Talia</name><name sortKey="Hill, Bradford G" sort="Hill, Bradford G" uniqKey="Hill B" first="Bradford G." last="Hill">Bradford G. Hill</name><name sortKey="Lancaster, Jack R" sort="Lancaster, Jack R" uniqKey="Lancaster J" first="Jack R." last="Lancaster">Jack R. Lancaster</name><name sortKey="Zhang, Jianhua" sort="Zhang, Jianhua" uniqKey="Zhang J" first="Jianhua" last="Zhang">Jianhua Zhang</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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