Abstract
Over evolutionary time, human mitochondrial DNA (mtDNA) has accumulated many mutations. Because mtDNA is exclusively inherited from the maternal lineage, these mtDNA mutations have given rise to different mtDNA genetic backgrounds, or haplogroups. Human mtDNA codes subunits of the oxidative phosphorylation system and the RNAs required for the expression of these subunits. As this cell pathway is significant in cell homeostasis, mtDNA population polymorphisms may affect cell function, tissue dynamics and, finally, the health status of individuals. Supporting this idea, transmitochondrial cell lines differ in cellular, biochemical and molecular-genetic properties among mtDNA haplogroups. Moreover, several epidemiological studies suggest that population genetic variation in mtDNA can have important phenotypic effects and modify the predisposition of human beings toward different disorders. Human mitogenomics, the study of mtDNAs in humans, will allow the development of mtDNA barcodes connecting particular mtDNA haplotypes with higher/lower propensity to particular diseases. Importantly, mitogenomics offers a previously neglected avenue for the development of drugs to treat individuals according their mtDNA genetic background, raising the possibility of mitochondrially-personalized medicine.
Keywords: Haplogroup, mitogenomics, MtDNA, OXPHOS, personalized medicine, Mitochondrial Genomic Variation, mutation, homeostasis, OXIDATIVE PHOSPHORYLATION, PHENOTYPIC EFFECTS
Current Pharmacogenomics and Personalized Medicine
Title: Mitogenomics: Recognizing the Significance of Mitochondrial Genomic Variation for Personalized Medicine
Volume: 9 Issue: 2
Author(s): Inigo Martinez-Romero, Sonia Emperador, Laura LLobet, Julio Montoya and Eduardo Ruiz-Pesini
Affiliation:
Keywords: Haplogroup, mitogenomics, MtDNA, OXPHOS, personalized medicine, Mitochondrial Genomic Variation, mutation, homeostasis, OXIDATIVE PHOSPHORYLATION, PHENOTYPIC EFFECTS
Abstract: Over evolutionary time, human mitochondrial DNA (mtDNA) has accumulated many mutations. Because mtDNA is exclusively inherited from the maternal lineage, these mtDNA mutations have given rise to different mtDNA genetic backgrounds, or haplogroups. Human mtDNA codes subunits of the oxidative phosphorylation system and the RNAs required for the expression of these subunits. As this cell pathway is significant in cell homeostasis, mtDNA population polymorphisms may affect cell function, tissue dynamics and, finally, the health status of individuals. Supporting this idea, transmitochondrial cell lines differ in cellular, biochemical and molecular-genetic properties among mtDNA haplogroups. Moreover, several epidemiological studies suggest that population genetic variation in mtDNA can have important phenotypic effects and modify the predisposition of human beings toward different disorders. Human mitogenomics, the study of mtDNAs in humans, will allow the development of mtDNA barcodes connecting particular mtDNA haplotypes with higher/lower propensity to particular diseases. Importantly, mitogenomics offers a previously neglected avenue for the development of drugs to treat individuals according their mtDNA genetic background, raising the possibility of mitochondrially-personalized medicine.
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Martinez-Romero Inigo, Emperador Sonia, LLobet Laura, Montoya Julio and Ruiz-Pesini Eduardo, Mitogenomics: Recognizing the Significance of Mitochondrial Genomic Variation for Personalized Medicine, Current Pharmacogenomics and Personalized Medicine 2011; 9 (2) . https://dx.doi.org/10.2174/187569211795508457
DOI https://dx.doi.org/10.2174/187569211795508457 |
Print ISSN 1875-6921 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6913 |
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