| Roles of mitochondria in human disease. | |
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MedLine Citation:
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PMID: 20533904 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The chapters throughout this volume illustrate the many contributions of mitochondria to the maintenance of normal cell and tissue function, experienced as the health of the individual. Mitochondria are essential for maintaining aspects of physiology as fundamental as cellular energy balance, the modulation of calcium signalling, in defining cellular redox balance, and they house significant biosynthetic pathways. Mitochondrial numbers and volume within cells are regulated and have an impact on their functional roles, while, especially in the CNS (central nervous system), mitochondrial trafficking is critical to ensure the cellular distribution and strategic localization of mitochondria, presumably driven by local energy demand. Maintenance of a healthy mitochondrial population involves a complex system of quality control, involving degrading misfolded proteins, while damaged mitochondria are renewed by fusion or removed by autophagy. It seems evident that mechanisms that impair any of these processes will impair mitochondrial function and cell signalling pathways, leading to disordered cell function which manifests as disease. As gatekeepers of cell life and cell death, mitochondria regulate both apoptotic and necrotic cell death, and so at its most extreme, disturbances involving these pathways may trigger untimely cell death. Conversely, the lack of appropriate cell death can lead to inappropriate tissue growth and development of tumours, which are also characterized by altered mitochondrial metabolism. The centrality of mitochondrial dysfunction to a surprisingly wide range of major human diseases is slowly becoming recognized, bringing with it the prospect of novel therapeutic approaches to treat a multitude of unpleasant and pervasive diseases. |
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Authors:
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Michael R Duchen; Gyorgy Szabadkai |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: Essays in biochemistry Volume: 47 ISSN: 1744-1358 ISO Abbreviation: Essays Biochem. Publication Date: 2010 |
Date Detail:
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Created Date: 2010-06-10 Completed Date: 2010-12-08 Revised Date: 2013-01-24 |
Medline Journal Info:
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Nlm Unique ID: 0043306 Medline TA: Essays Biochem Country: England |
Other Details:
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Languages: eng Pagination: 115-37 Citation Subset: IM |
Affiliation:
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Department of Cell and Developmental Biology and Consortium for Mitochondrial Research, University College London, Gower Street, London WC1E 6BT, UK. m.duchen@ucl.ac.uk |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Cell Death
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physiology Central Nervous System / cytology, metabolism Humans Mitochondria / metabolism* Models, Biological Signal Transduction / physiology* |
| Grant Support | |
ID/Acronym/Agency:
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089698//Wellcome Trust; G-0905//Parkinson's UK; //Medical Research Council; //Wellcome Trust |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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