Title |
Altering the balance between healthy and mutated mitochondrial DNA
|
---|---|
Published in |
Journal of Inherited Metabolic Disease, May 2010
|
DOI | 10.1007/s10545-010-9122-6 |
Pubmed ID | |
Authors |
Paul M. Smith, Robert N. Lightowlers |
Abstract |
Pathogenic mutations of the mitochondrial genome are frequently found to co-exist with wild-type mtDNA molecules, a state known as heteroplasmy. In most disease cases, the mutation is recessive with manifestation of a clinical phenotype occurring when the proportion of mutated mtDNA exceeds a high threshold. The concept of increasing the ratio of healthy to mutated mtDNA as a means to correcting the biochemical defect has received much attention. A number of strategies are highlighted in this article, including manipulation of the mitochondrial genome by antigenomic drugs or restriction endonucleases, zinc finger peptide-targeted nucleases and exercise-induced gene shifting. The feasibility of these approaches has been demonstrated in a number of models, however more work is necessary before use in human patients. |
Mendeley readers
Geographical breakdown
Country | Count | As % |
---|---|---|
United States | 1 | 2% |
Canada | 1 | 2% |
Unknown | 44 | 96% |
Demographic breakdown
Readers by professional status | Count | As % |
---|---|---|
Student > Ph. D. Student | 11 | 24% |
Student > Bachelor | 8 | 17% |
Researcher | 6 | 13% |
Professor > Associate Professor | 6 | 13% |
Student > Master | 5 | 11% |
Other | 5 | 11% |
Unknown | 5 | 11% |
Readers by discipline | Count | As % |
---|---|---|
Agricultural and Biological Sciences | 14 | 30% |
Medicine and Dentistry | 10 | 22% |
Biochemistry, Genetics and Molecular Biology | 9 | 20% |
Neuroscience | 3 | 7% |
Sports and Recreations | 2 | 4% |
Other | 3 | 7% |
Unknown | 5 | 11% |