Abstract
Background and Aims: Mitochondrial dysfunction is considered a mechanistic factor in a number of pathologies, including atherosclerosis. It is known that mutations and defects of mitochondrial DNA (mtDNA) underlie such diseases. Mitochondrial editing is a desirable approach for the therapy of mitochondrial related diseases. The main problem in creating approach to mtDNA editing is the complexity of targeted delivery of macromolecular complexes to mitochondria. The aim of our study is to create a vector that is able to at least cut mtDNA in specific manner or even to edit mtDNA.
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