Progress and prospects: gene therapy for mitochondrial DNA disease
Open accessAbstract
Defects of the mitochondrial genome cause a wide variety of clinical disorders. Except for rare cases where surgery or transplant is indicated, there is no effective treatment for patients. Genetic-based therapies are consequently being considered. On account of the difficulties associated with mitochondrial (mt) transfection, alternative approaches whereby mitochondrial genes can be engineered and introduced into the nucleus (allotopic expression) are being attempted with some success, at least in cultured cells. Defects in the activities of multi-subunit complexes of the oxidative phosphorylation apparatus have been circumvented by the targeted expression of simple single subunit enzymes from other species (xenotopic expression). Although far from the clinic, these approaches show promise. Similarly, nuclear transfection with genes encoding restriction endonucleases or sequence-specific zinc finger-binding proteins destined for mitochondria has also proved successful in targeting mtDNA-borne pathogenic mutations. This is particularly important, as mutated mtDNA is often found in cells that also contain normal copies of the genome, a situation termed heteroplasmy. Shifting the levels of heteroplasmy towards the normal mtDNA has become the goal of a variety of invasive and non-invasive methods, which are also highlighted in this review.
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CMCO:PNA hybrid molecules have been successfully targeted and imported into mitochondria in whole cells.
“Molecules with greater polarity have since been designed (cell membrane crossing oligomers, CMCOs), and CMCO:PNA hybrid molecules have been successfully targeted and imported into mitochondria in whole cells [235].”
From Mitochondrial DNA mutations and human disease (2010) · cites this paper as [235]
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- Authors
- Kyriakouli, D. S., Boesch, P., Taylor, R. W., & Lightowlers, R. N.
- Affiliations
- Newcastle University (GB)
- Corresponding author
- Lightowlers, R N
- Venue
- Gene Therapy
- Published
- 2008-05-22
- Volume
- 15
- Issue
- 14
- Pages
- 1017-1023
- ISSN
- 0969-7128 (ISSN-L)
- 1476-5462
- OpenAlex
- W2090669387
- Cited by
- 76
- References
- 22
- Citations by year
- 2026: 1 · 2025: 1 · 2023: 2 · 2021: 1 · 2019: 4 · 2018: 4 · 2017: 3 · 2016: 5 · 2015: 5 · 2014: 4 · 2013: 4 · 2012: 10
- FWCI
- 4.38
- Type
- journal article
- Language
- en
- Open access
- green
- doi.org
- Locations
- Gene Therapy (publishedVersion)
- PubMed (publishedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Funders
- Wellcome Trust (074454, 078900)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › CRISPR and Genetic Engineering
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Virus-based gene therapy research
- Keywords
- mitochondrial DNA disease, allotopic expression, oxidative phosphorylation, heteroplasmy, restriction enzymes, zinc finger proteins
- MeSH terms
- DNA, Mitochondrial, Humans, Mutation, Genetic Therapy, Gene Expression, Gene Transfer Techniques, Gene Targeting, Mitochondrial Diseases
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