The contribution of mitochondrial DNA alterations to aging, cancer, and neurodegeneration
Mitochondrial DNA (mtDNA) is as a double-stranded molecule existing in hundreds to thousands copies in cells depending on cell metabolism and exposure to endogenous and/or environmental stressors. The coordination of mtDNA replication and transcription regulates the pace of mitochondrial biogenesis...
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| Vydáno v: | Experimental gerontology Ročník 178; s. 112203 |
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| Médium: | Journal Article |
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Elsevier Inc
01.07.2023
Elsevier |
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| ISSN: | 0531-5565, 1873-6815, 1873-6815 |
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| Abstract | Mitochondrial DNA (mtDNA) is as a double-stranded molecule existing in hundreds to thousands copies in cells depending on cell metabolism and exposure to endogenous and/or environmental stressors. The coordination of mtDNA replication and transcription regulates the pace of mitochondrial biogenesis to guarantee the minimum number of organelles per cell. mtDNA inheritance follows a maternal lineage, although bi-parental inheritance has been reported in some species and in the case of mitochondrial diseases in humans. mtDNA mutations (e.g., point mutations, deletions, copy number variations) have been identified in the setting of several human diseases. For instance, sporadic and inherited rare disorders involving the nervous system as well higher risk of developing cancer and neurodegenerative conditions, including Parkinson's and Alzheimer's disease, have been associated with polymorphic mtDNA variants. An accrual of mtDNA mutations has also been identified in several tissues and organs, including heart and muscle, of old experimental animals and humans, which may contribute to the development of aging phenotypes. The role played by mtDNA homeostasis and mtDNA quality control pathways in human health is actively investigated for the possibility of developing targeted therapeutics for a wide range of conditions.
•Mitochondrial DNA (mtDNA) is a multi-copy genome varying with cell metabolism and stressors.•Heteroplasmic and homoplasmic mtDNA mutations contribute to several disease conditions.•Sporadic and inherited rare disorders of the nervous system hold mtDNA mutations.•Accrual of mtDNA mutations has been reported in several tissues during aging.•mtDNA mutations are implicated in tumorigenesis. |
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| AbstractList | Mitochondrial DNA (mtDNA) is as a double-stranded molecule existing in hundreds to thousands copies in cells depending on cell metabolism and exposure to endogenous and/or environmental stressors. The coordination of mtDNA replication and transcription regulates the pace of mitochondrial biogenesis to guarantee the minimum number of organelles per cell. mtDNA inheritance follows a maternal lineage, although bi-parental inheritance has been reported in some species and in the case of mitochondrial diseases in humans. mtDNA mutations (e.g., point mutations, deletions, copy number variations) have been identified in the setting of several human diseases. For instance, sporadic and inherited rare disorders involving the nervous system as well higher risk of developing cancer and neurodegenerative conditions, including Parkinson's and Alzheimer's disease, have been associated with polymorphic mtDNA variants. An accrual of mtDNA mutations has also been identified in several tissues and organs, including heart and muscle, of old experimental animals and humans, which may contribute to the development of aging phenotypes. The role played by mtDNA homeostasis and mtDNA quality control pathways in human health is actively investigated for the possibility of developing targeted therapeutics for a wide range of conditions.Mitochondrial DNA (mtDNA) is as a double-stranded molecule existing in hundreds to thousands copies in cells depending on cell metabolism and exposure to endogenous and/or environmental stressors. The coordination of mtDNA replication and transcription regulates the pace of mitochondrial biogenesis to guarantee the minimum number of organelles per cell. mtDNA inheritance follows a maternal lineage, although bi-parental inheritance has been reported in some species and in the case of mitochondrial diseases in humans. mtDNA mutations (e.g., point mutations, deletions, copy number variations) have been identified in the setting of several human diseases. For instance, sporadic and inherited rare disorders involving the nervous system as well higher risk of developing cancer and neurodegenerative conditions, including Parkinson's and Alzheimer's disease, have been associated with polymorphic mtDNA variants. An accrual of mtDNA mutations has also been identified in several tissues and organs, including heart and muscle, of old experimental animals and humans, which may contribute to the development of aging phenotypes. The role played by mtDNA homeostasis and mtDNA quality control pathways in human health is actively investigated for the possibility of developing targeted therapeutics for a wide range of conditions. Mitochondrial DNA (mtDNA) is as a double-stranded molecule existing in hundreds to thousands copies in cells depending on cell metabolism and exposure to endogenous and/or environmental stressors. The coordination of mtDNA replication and transcription regulates the pace of mitochondrial biogenesis to guarantee the minimum number of organelles per cell. mtDNA inheritance follows a maternal lineage, although bi-parental inheritance has been reported in some species and in the case of mitochondrial diseases in humans. mtDNA mutations (e.g., point mutations, deletions, copy number variations) have been identified in the setting of several human diseases. For instance, sporadic and inherited rare disorders involving the nervous system as well higher risk of developing cancer and neurodegenerative conditions, including Parkinson's and Alzheimer's disease, have been associated with polymorphic mtDNA variants. An accrual of mtDNA mutations has also been identified in several tissues and organs, including heart and muscle, of old experimental animals and humans, which may contribute to the development of aging phenotypes. The role played by mtDNA homeostasis and mtDNA quality control pathways in human health is actively investigated for the possibility of developing targeted therapeutics for a wide range of conditions. Mitochondrial DNA (mtDNA) is as a double-stranded molecule existing in hundreds to thousands copies in cells depending on cell metabolism and exposure to endogenous and/or environmental stressors. The coordination of mtDNA replication and transcription regulates the pace of mitochondrial biogenesis to guarantee the minimum number of organelles per cell. mtDNA inheritance follows a maternal lineage, although bi-parental inheritance has been reported in some species and in the case of mitochondrial diseases in humans. mtDNA mutations (e.g., point mutations, deletions, copy number variations) have been identified in the setting of several human diseases. For instance, sporadic and inherited rare disorders involving the nervous system as well higher risk of developing cancer and neurodegenerative conditions, including Parkinson's and Alzheimer's disease, have been associated with polymorphic mtDNA variants. An accrual of mtDNA mutations has also been identified in several tissues and organs, including heart and muscle, of old experimental animals and humans, which may contribute to the development of aging phenotypes. The role played by mtDNA homeostasis and mtDNA quality control pathways in human health is actively investigated for the possibility of developing targeted therapeutics for a wide range of conditions. •Mitochondrial DNA (mtDNA) is a multi-copy genome varying with cell metabolism and stressors.•Heteroplasmic and homoplasmic mtDNA mutations contribute to several disease conditions.•Sporadic and inherited rare disorders of the nervous system hold mtDNA mutations.•Accrual of mtDNA mutations has been reported in several tissues during aging.•mtDNA mutations are implicated in tumorigenesis. |
| ArticleNumber | 112203 |
| Author | Calvani, Riccardo Leeuwenburgh, Christiaan Coelho-Júnior, Hélio José Guerra, Flora Bucci, Cecilia Picca, Anna Marzetti, Emanuele |
| Author_xml | – sequence: 1 givenname: Anna surname: Picca fullname: Picca, Anna organization: Department of Medicine and Surgery, LUM University, 70100 Casamassima, Italy – sequence: 2 givenname: Flora surname: Guerra fullname: Guerra, Flora organization: Department of Biological and Environmental Sciences and Technologies, University of Salento, 73100 Lecce, Italy – sequence: 3 givenname: Riccardo surname: Calvani fullname: Calvani, Riccardo email: riccardo.calvani@unicatt.it organization: Fondazione Policlinico Universitario “Agostino Gemelli” IRCCS, 00168 Rome, Italy – sequence: 4 givenname: Hélio José surname: Coelho-Júnior fullname: Coelho-Júnior, Hélio José organization: Department of Geriatrics and Orthopedics, Università Cattolica del Sacro Cuore, 00168 Rome, Italy – sequence: 5 givenname: Christiaan surname: Leeuwenburgh fullname: Leeuwenburgh, Christiaan organization: Department of Physiology and Aging, University of Florida, 32601 Gainesville, FL, USA – sequence: 6 givenname: Cecilia surname: Bucci fullname: Bucci, Cecilia organization: Department of Biological and Environmental Sciences and Technologies, University of Salento, 73100 Lecce, Italy – sequence: 7 givenname: Emanuele surname: Marzetti fullname: Marzetti, Emanuele organization: Fondazione Policlinico Universitario “Agostino Gemelli” IRCCS, 00168 Rome, Italy |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/37172915$$D View this record in MEDLINE/PubMed |
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| Title | The contribution of mitochondrial DNA alterations to aging, cancer, and neurodegeneration |
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